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Resumo Introdução: O acidente vascular cerebral isquêmico tem como tratamento a terapia trombolítica, aplicada ainda na fase aguda, promovendo melhora importante nas sequelas acarretadas por este agravo. Considerando a complexidade da terapia trombolítica, torna-se necessário que os enfermeiros compreendam suas competências para auxiliar no cuidado. Objetivo: Identificar evidências científicas acerca das competências do enfermeiro no cuidado a pacientes com acidente vascular cerebral elegíveis à terapia trombolítica. Metodologia: Revisão integrativa composta por seis etapas em seis etapas (elaboração da questão, busca na literatura, coleta de dados, análise, discussão e apresentação da revisão), realizada nas bases de dados MEDLINE, LILACS, BDENF, IBECS, PubMed, Scopus, Web of Science, Embase e CINAHL. A busca foi realizada entre agosto e setembro de 2022 adotando como critérios de inclusão estudos primários; gratuitos, disponíveis eletronicamente na íntegra; nos idiomas inglês, português e espanhol. Foram obtidos inicialmente 2.830 estudos, os quais passaram por uma seleção, onde foram incluídos aqueles que atendiam os critérios previamente estabelecidos. Resultados: Com base nos doze estudos incluídos nesta revisão identificaram-se competências voltadas à três atividades do cuidado: gestão do cuidado como trabalho em equipe, códigos, fluxos e protocolos, assistência ao paciente antes, durante e após a utilização da terapia trombolítica e educação em saúde para equipe, pacientes e familiares. Conclusão: Os achados desta revisão puderam evidenciar as competências do enfermeiro no cuidado aos pacientes elegíveis a terapia trombolítica, as quais perpassam diferentes áreas de atuação do enfermeiro. Para este estudo prevaleceram as competências assistências, seguida por competências gerenciais.
Resumen Introducción: El accidente cerebrovascular isquémico se trata con terapia trombolítica, aplicada incluso en la fase aguda, que promueve una mejoría significativa de las secuelas provocadas por este padecimiento. Considerando la complejidad de la terapia trombolítica, es necesario que las personas profesionales de enfermería comprendan sus competencias para ayudar en el cuidado. Objetivo: Identificar evidencias científicas sobre las competencias del personal de enfermería en el cuidado de pacientes con accidente cerebrovascular elegibles para terapia trombolítica. Metodología: Revisión integradora que consta de seis etapas (elaboración de la pregunta, búsqueda bibliográfica, recolección de datos, análisis, discusión y presentación de la revisión), realizada en las bases de dados MEDLINE, LILACS, BDENF, IBECS, PubMed, Scopus, Web of Science, Embase y CINAHL. La búsqueda se realizó entre agosto y septiembre de 2022. Los criterio de inclusión fueron: estudios primarios, gratuito, disponible electrónicamente en su totalidad, en inglés, portugués y español. Inicialmente se obtuvieron 2830 estudios, los cuales fueron sometidos a un proceso de selección, que incluyó aquellos que cumplían con los criterios previamente establecidos. Resultados: A partir de los doce estudios incluidos en esta revisión, se identificaron competencias centradas en tres actividades asistenciales: gestión del cuidado como trabajo en equipo, códigos, flujos y protocolos, atención a pacientes antes, durante y después del uso de la terapia trombolítica y educación en salud para personal, pacientes y familias. Conclusión: Los hallazgos de esta revisión pudieron resaltar las competencias de las personas profesionales en enfermería en el cuidado de personas elegibles para terapia trombolítica, que abarcan diferentes áreas de actuación del personal de enfermería. Para este estudio, prevalecieron las habilidades asistenciales, seguidas de las competencias gerenciales.
ABSTRACT Introduction: Ischemic stroke is treated with thrombolytic therapy, applied even in the acute phase, promoting a significant improvement in the after-effects caused by this condition. Considering the complexity of thrombolytic therapy, it is necessary for nurses to understand the skills required to assist in care. Objective: To identify scientific evidence about the competencies of nurses in the care of patients with stroke who are eligible for thrombolytic therapy. Methodology: An integrative review consisting of six stages (elaboration of the question, literature review, data collection, analysis, discussion, and presentation), conducted in MEDLINE, LILACS, BDENF, IBECS, PubMed, Scopus, Web of Science, Embase, and CINAHL databases. The search was carried out between August and September 2022 using primary studies as the inclusion criteria: free of charge, fully available electronically, published in English, Portuguese, or Spanish. Initially, 2.830 studies were obtained, which underwent a selection process that included only those studies that met the previously established criteria. Results: Based on the twelve studies included in this review, competencies focused on three care activities were identified: care management such as teamwork; codes; flows and protocols; patient care before, during, and after the use of thrombolytic therapy; and education health education for staff, patients, and families. Conclusion: The findings of this review highlighted the nurses' competencies in the care of patients eligible for thrombolytic therapy, which encompass different areas of the nurse's work. For this study, assistance competencies prevailed, followed by management competencies.
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Humans , Thrombolytic Therapy/nursing , Stroke/nursing , Nursing CareРеферат
Objective:Based on the Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)signaling pathway,to explore the influences of Liyan syrup on pharyngeal tissue injury and pharyngeal mucosal repair in rats with chronic phar-yngitis.Methods:SD rats were randomly separated into control group,model group,Liyan syrup group,RO8191(JAK2/STAT3 acti-vator)group,Liyan syrup+RO8191 group,the model group and drug intervention group were treated with ammonia water to stimulate the pharynx to build a chronic pharyngitis model,while rats in control group were injected with an equal dose of normal saline into the pharynx.After the intervention of Liyan Syrup and RO8191,the general condition of rats and the apparent state of pharynx were detected,and the apparent state of pharynx was scored;the pathological changes of pharynx of rats were measured by HE staining;the proportions of CD4+T and CD8+T and the ratio of CD4+T/CD8+T in peripheral blood T lymphocyte subsets of rats were measured by flow cytometry;the levels of serum tumor necrosis factor alpha(TNF-α),IL-6,IL-10,malondialdehyde(MDA),reactive oxygen species(ROS)and total antioxidant capacity(T-AOC)were measured by kits;the expressions of JAK2/STAT3 pathway-related proteins in rat pharyngeal tissues were measured by immunoblotting.Results:Compared with control group,the pharyngeal tissue of model group showed obvious pathological morphological damage,the peripheral blood CD4+T proportion and CD4+T/CD8+T,IL-10 and serum T-AOC level decreased(P<0.05),the pharyngeal appearance state score,CD8+T ratio,serum TNF-α,IL-6,MDA and ROS levels,and pharyngeal tissue p-JAK2/JAK2 and p-STAT3/STAT3 levels increased(P<0.05);compared with model group and Liyan syrup+ RO8191 group,the pathological and morphological damage of the pharynx of rats in Liyan syrup group was alleviated,the peripheral blood CD4+T and CD4+T/CD8+T,IL-10,and serum T-AOC level all increased(P<0.05),and the pharyngeal appearance state score,CD8+T,serum TNF-α,IL-6,MDA and ROS levels,and pharyngeal tissue p-JAK2/JAK2 and p-STAT3/STAT3 levels all decreased(P<0.05);the change trend of each index in RO8191 group was opposite to that in Liyan syrup group.Conclusion:Liyan syrup can reduce inflammation and oxidative stress by inhibiting the activation of JAK2/STAT3 signal,enhance anti-inflammatory and antioxidant capacity,relieve throat tissue damage and repair pharyngeal mucosa in rats with chronic pharyngitis.
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Objective:To investigate the effect and mechanism of Grifola frondosa extract on inflammatory response of colon tissue in rats with ulcerative colitis(UC)by regulating interleukin-6(IL-6)/Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods:Forty SD rats were randomly divided into blank control group,UC model group,Grifola frondosa treatment group,western medicine treatment group and combined treatment group,with 8 rats in each group.After UC rats were established by free drinking 3%DSS for 7 days,the treatment group were given Grifola frondosa extract 10 mg/(kg·d),sulfasalazine 0.3 g/(kg·d),and the same amount of two drugs,for 14 consecutive days.During the experiment,general state of rats were observed,and the disease activity index(DAI)score was calculated;pathological changes of rats colon tissue were observed by HE staining;protein expression levels of IL-6,JAK2,STAT3 and p-STAT3 in rats colon tissue were detected by Western blot;content of IL-6 in rats serum was detected by ELISA;protein contents and expressions of IL-6R and MPO in rats colon tissue were determined by immunohistochemistry.Results:Compared with blank control group,general state of rats in UC model group was poor,DAI score was increased,obvious tissue mucosal defects and inflammatory cell infiltration were observed by HE staining;protein expression levels of IL-6,JAK2,STAT3 and p-STAT3 in rats colon tissue and contents of IL-6R and MPO were significantly increased(P<0.01);content of IL-6 in rats serum was significantly increased(P<0.01),the difference was statistically significant.Compared with UC model group,general condition of rats in each treatment group was improved,DAI score was decreased,HE staining showed that mucosal defects were improved to varying degrees,and occasionally inflammatory cell infiltration was observed;protein expression levels of IL-6,JAK2,STAT3 and p-STAT3 in colon tissue were significantly decreased(P<0.01),contents of IL-6R and MPO in colon tissue and content of IL-6 in serum were significantly decreased(P<0.01 or P<0.05),the differences were statistically significant.Conclusion:Grifola frondosa extract can reduce the inflammatory response in colon tissue of UC rats by regulating expressions of IL-6/JAK2/STAT3 signaling pathway related factors.
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Objective To explore the correlation of nerve function and prognosis with serum uric acid(UA),homocysteine(Hcy)and low-density lipoprotein cholesterol(LDL-C)in patients with acute cerebral infarction(ACI)after alteplase intravenous thrombolysis.Methods A total of 220 ACI patients undergoing thrombolysis in Changsha First Hospital ICU between January 2020 and December 2022 were enrolled,and according to mRS score at 3 months after thrombolysis,they were divided into poor prognosis group(mRS score＞2,91 cases)and good prognosis group(mRS score ≤2,129 cases).The serum levels of UA,Hcy and LDL-C were compared between the two groups.The correlation between the three indexes and score of National Institutes of Health Stroke Scale(NIHSS),and their predictive value for poor prognosis were analyzed.Results At 1 and 3 d after thrombolysis,the serum levels of UA,Hcy and LDL-C and NIHSS score were sig-nificantly decreased in both groups,and the serum levels of UA and Hcy and NIHSS score at 3 d after thrombolysis were significantly lower than those at 1 d(P＜0.05).The poor prognosis group had obviously higher serum levels of UA,Hcy and LDL-C and NIHSS score at 1 and 3 d after thrombolysis than the good prognosis group(P＜0.05,P＜0.01).Pearson correlation analysis showed that the serum levels of UA,Hcy and LDL-C were positively correlated with NIHSS score at 1 and 3 d after thrombolysis(P＜0.01).ROC curve analysis indicated that the AUC values of UA,Hcy and LDL-C at 1 d after thrombolysis for predicting poor prognosis were 0.707(95％CI:0.639-0.776),0.800(95％CI:0.739-0.860)and 0.624(95％CI:0.550-0.698),respectively,while the values of them at 3 d after thrombolysis were 0.655(95％CI:0.583-0.726),0.730(95％CI:0.664-0.795)and 0.573(95％CI:0.497-0.649),respectively.Conclusion In ACI patients after thrombolysis,the serum levels of UA,Hcy and LDL-C are increased in those with poor prognosis,and are associated with the severity of nerve injury.The levels at 1 d after throm-bolysis have good predictive value for poor prognosis.
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Objective To explore the effects of intravenous thrombolysis combined with Solitaire FR stent thrombectomy on vascular recanalization,neurologic function and prognosis in patients with acute cerebral infarction(ACI)due to large artery occlusion(LAO).Methods A total of 172 patients with ACI-LAO treated in our department between October 2020 and March 2023 were retrospectively enrolled.According to treatment regimens,they were assigned into control group(86 cases,alteplase intravenous thrombolysis)and study group(86 cases,alteplase intravenous thrombolysis combined with Solitaire FR stent thrombectomy).Vascular recanalization,neurolog-ic function,cerebral perfusion and occurrence of adverse events were compared between the two groups.After 90 d of follow-up,their prognosis was evaluated with modified Rankin scale.Results There was no significant difference in success rate of vascular recanalization between the two group(P＞0.05),but complete recanalization rate was statistically higher in the study group than the control group(68.60％vs 50.00％,P＜0.05).The study group had obviously lower NHISS scores at 7 and 14 d after treatment,higher cerebral blood volume and cerebral blood flow,but shorter mean transit time when compared with the control group(P＜0.05,P＜0.01).No notable difference was observed in the total incidence of adverse events between them(P＞0.05).After 90 d of follow-up,the proportion of good prognosis was higher in the study group than the control group(80.23％vs 63.95％,P＜0.05).Conclusion Intravenous thrombolysis combined with Soli-taire FR stent thrombectomy shows better efficacy in ACI-LAO patients,with better vascular re-canalization and great improvements in neurologic function and prognosis.
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Objective To investigate the effect of electroacupuncture preconditioning on microglia polarization in rats after cerebral ischemia reperfusion(IR)injury and explore the role of tyrosine kinase 2(J AK2)/signal transducer and activator of transcription 3(STAT3)pathway in the process.Methods Forty-five clean-grade healthy male Sprague-Dawley rats were randomly and equally divided into sham operation group,IR group and electroacupuncture preconditioning group.Rat model of IR injury was induced with thread occlusion of the internal carotid artery.Before modeling,electroacupuncture preconditioning was applied to Baihui acupoint for 5 consec-utive days in the preconditioning group,and exposure of the cervical blood vessels were inflicted in the sham-operation group.At 24 h after reperfusion,the severity of neurological deficit was observed by modified neurological deficit score(mNSS),and the cerebral infarct volume was observed by TTC staining.Western blotting was used to detect the protein levels of classical acti-vated type(M1)marker inducible nitric oxide synthase(iNOS),alternative activated type(M2)marker arginase 1(Arg-1),JAK2 and p-JAK2,and STAT3 and p-STAT3,and q-PCR was applied to detect the mRNA expression of iNOS and Arg-1.The expression of TNF-α and IL-10 was measured by ELISA.Results Compared with the sham operation group,the mNSS,infarct vol-ume,protein levels of p-JAK2/JAK2,p-STAT3/STAT3,protein and mRNA levels of iNOS and Arg-1,and expression of TNF-α and IL-10 were significantly increased in the IR and electroacu-puncture preconditioning groups(P＜0.01).The preconditioning group had obviously lower mNSS,smaller infarct volume,decreased protein levels of p-JAK2/JAK2,p-STAT3/STAT3,re-duced protein and mRNA levels of iNOS,and declined TNF-α expression,but elevated expression of Arg-1 at protein(2.0±0.2 vs 1.5±0.1)and mRNA(4.2±0.8 vs 3.1±0.3)levels and increased IL-10 expression(49.1±7.1 pg/mg vs 27.9±5.9 pg/mg)when compared with the IR group(P＜0.01).Conclusion Electroacupuncture preconditioning can promote the polarization of microglia to M2 and inhibit the polarization of microglia to M1 after cerebral IR injury,which may be relat-ed to the inhibition of JAK2/STAT3 pathway.
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ObjectiveTo explore host factors interacting with influenza virus nucleoprotein （NP） and study their effects on influenza virus replication， as well as the mechanism of gardenia jasminoides iridoid glycoside （IGE） in inhibiting influenza virus. MethodA yeast two-hybrid system was utilized to screen host factors that interacted with influenza virus NP. Heterogeneous nuclear ribonucleoprotein D0 （HNRNPD）， glucosamine-6-phosphate deaminase 1 （GNPDA1）， poly（rC）-binding protein 1 （PCBP1）， and protein inhibitor of activated signal transducer and activator of transcription （STAT） protein 1 （PIAS1） were validated by immunoprecipitation assay. The effects of PIAS1 and HNRNPD on influenza virus replication were compared by a dual luciferase assay， and the effects of IGE on influenza virus replication were examined in the presence of transfected ribonucleoprotein （RNP） and knockdown of PIAS1. ICR mice were randomly divided into a normal group， model group， oseltamivir phosphate group， and high， medium， and low dose IGE groups， with 10 mice in each group. In addition to the normal group， each group was infected with the influenza A virus FM1 strain by nasal drip to establish a viral pneumonia model. The high， medium， and low dose IGE groups were given drugs of 50， 25， and 12.5 mg∙kg-1 by gavage， and the oseltamivir phosphate group was given the drug of 27.5 mg∙kg-1 by gavage. Equal amounts of distilled water were instilled in the normal and model groups for four consecutive days. Later， protein expression of PIAS1， NP， phosphorylated （p）-STAT3， STAT3， p-STAT1， and STAT1 were detected in the lung tissue by Western blot. ResultIn yeast two-hybrid assays， 16 potential host targets interacting with influenza virus NP were identified. Immunoprecipitation experiments revealed that HNRNPD and PIAS1 could interact with influenza virus NP. The dual luciferase reporter assays found that both PIAS1 knockdown and overexpression significantly affected IAV RNP activity （P<0.05， P<0.01）， and the effect of HNRNPD on IAV RNP was not significant. Both high and low dose IGE groups reduced influenza virus replication （P<0.05） and reversed the increase in influenza virus replication caused by the knockdown of PIAS1（P<0.05， P<0.01）. The expressions of PIAS1， NP， p-STAT3， p-STAT1， and STAT1 in the lung tissue of infected mice were reduced to different degrees in each IGE group （P<0.05， P<0.01）. ConclusionPIAS1 interacts with influenza virus NP and is able to inhibit influenza virus replication. IGE may exert antiviral effects by inhibiting the activity of IAV RNP through the PIAS1/STAT1 pathway.
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ObjectiveTo explore the possible mechanism of Changweiqing （肠胃清） in the treatment of colorectal cancer. MethodsHCT 116 cancer cells were used to prepare intestinal cancer cells with silenced polypyrimidine region binding protein 3 （PTBP3） gene and stably transfected cells with overexpressed PTBP3 gene. Stably transfected cells with silenced PTBP3， stably transfected cells with overexpressed PTBP3 and untransfected cancer cells were injected into the armpit of 72 nude mice to construct three different subcutaneous transplanted tumor models of colorectal cancer cells， including the silenced model， the overexpressed model and the control model， with 24 mice per model. Mice of each transplanted tumor modelwere randomly divided into Changweiqing （CWQ） group， oxaliplatin （OXA） group and normal saline （NS） group， with 8 mice in each group. The CWQ groups were given intragastric administration of 35.9625 g/kg of Changweiqing oral liquid and were intraperitoneally injected with 0.2ml of normal saline； the NS groups were given 0.5ml of normal saline by gavage， and intraperitoneal injection of 0.2ml of normal saline； the OXA groups were intraperitoneally injected with 5 mg/kg （0.2 ml） of oxaliplatin and given 0.5ml of normal saline by gavage. Each group was given intragastric administration once a day and intraperitoneal injection three times a week. After 31 days， the weight of subcutaneous tumors in each group was measured， and the tumor inhibition rate of the groups in each model were measured. Immunohistochemistry and other methods were used to detect the expression level of cell proliferation cell nuclear antigen Ki67 and apoptosis index. Real-time PCR and Western Blot were used to detect mRNA and protein expressions of PTBP3， signal transducer and activator of transcription 3 （STAT3） splicing isoform α （STAT3α）， STAT3 splicing isoform β （STAT3β）， B-cell lymphoma/leukemia-2 （Bcl-2） splicing isoform α （Bcl-2α）， and Bcl-2 splicing isoform β （Bcl-2β） in subcutaneous tumor cells in each group. ResultsFor all three transplanted tumor models， the weight of the subcutaneous tumors and Ki67 expression level of subcutaneous tumor tissue in all CWQ groups and OXA groups were lower than those of the corresponding NS groups， while the apoptosis level were higher （P＜0.05 or P＜0.01）. The mRNA and protein expressions of PTBP3， STAT3α， and Bcl-2α in the subcutaneous tumor tissues of the silenced model CWQ group and the overexpressed model CWQ group were lower than those of the corresponding NS groups， while the mRNA and protein expression levels of STAT3β and Bcl-2β were higher （P＜0.05 or P＜0.01）. All there groups of silenced model had lower subcutaneous tumor weight， Ki67 expression level， and mRNA and protein expression levels of PTBP3， STAT3α， and Bcl-2α in subcutaneous tumor tissue， as well as higher apoptosis level and mRNA and protein expression levels of STAT3β and Bcl-2β than those in all groups of control model； all groups of overexpressed model had higher subcutaneous tumor weight， Ki67 expression level， and mRNA and protein expression levels of PTBP3， STAT3α， and Bcl-2α ， while lower apoptosis level and mRNA and protein expression levels of STAT3β and Bcl-2β than those in all control model groups （P＜0.05 or P＜0.01）. In the control model， compared with the NS group， The tumor inhibition rate of all OXA groups was higher than that of corresponding CWQ groups， respectively. Compared to that of each control model group， the tumor inhibition rate was positive value of each silenced model group， and negative value of each overexpressed model group. ConclusionPTBP3 can promote the proliferation and inhibit apoptosis of intestinal cancer cells， upregulate the expression of STAT3α and Bcl-2α， and downregulate the expression of STAT3β and Bcl-2β in intestinal cancer cells. The meachnism of action of Changweiqing in the treatment of colorectal cancer maybe related to the inhibition of PTBP3， and regulation of the expression of STAT3α， STAT3β， Bcl-2α， and Bcl-2β.
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ObjectiveTo investigate the possible mechanism of Quyu Jiedu Formula （祛瘀解毒方） in the treatment of endometriosis in terms of iron autophagy mediated by nuclear receptor coactivator 4/nuclear factor κB （NCOA4/NF-κB） signalling pathway. MethodsFifty female SD rats were randomly divided into sham surgery group， model group， mifepristone group， low- and high-dose Quyu Jiedu Formula group， with 10 rats in each group. In the sham surgery group， only operation of opening and closing abdomen was performed， and in the remaining groups， the rat with endometriosis was modelled by autotransplantation. On the next day after successful modelling， saline 2 ml/d was given by gavage to the sham surgery group and the model group； mifepristone 1.05 mg/（kg·d） was given by gavage to the mifepristone group； Quyu Jiedu Formula 12.23 g/（kg·d） and 48.92 g/（kg·d） were given to the low- and high-dosage Quyu Jiedu Formula groups， respectively administered for 4 weeks consecutively. In the remaining 4 groups， all ectopic endometrial tissues were removed from the rats. The volume of ectopic lesions was measured in the model group， the mifepristone group， and the low- and high-dose Quyu Jiedu Formula groups， and the pathological changes of endometrial/ectopic tissues were observed by HE staining， and the protein expression and expression of NCOA4， Ferritin Heavy Chain 1 （FTH1）， Panax quinquefolium （P62）， Microtubule-associated Protein 1 Light Chain 3β （LC3B）， and P-NF-κB protein expression and NCOA4， FTH1， LC3B， P62 mRNA expression were detected in the endometrium and ectopic tissues； the co-localisation of NCOA4 and LC3B， free iron content， and levels of interleukin 6 （IL-6） and tumour necrosis factor α （TNF-α） in endometrial/eutopic endometrial tissues were also detected. ResultsNo ectopic lesions were seen in the sham surgery group. The ectopic tissues of rats in the model group showed obvious pathological damage， while the pathological damage of the ectopic tissues of rats in each admi-nistration group was reduced to different degrees. Compared with the model group， the volume of ectopic lesions was reduced in the mifepristone group and the high- and low-dose Quyu Jiedu Formula groups， and the volume of ectopic lesions in the high-dose Quyu Jiedu Formula group and the mifepristone group was significantly smaller than that in the low-dose Quyu Jiedu Formula group （P＜0.01）. Compared with the sham surgery group， the ectopic tissues of the model group showed up-regulation of LC3BⅡ/LC3B I values， NCOA4， and P-NF-κB protein expression， down-regulation of P62 and FTH1 protein expression， increase in free iron content and IL-6 and TNF-α levels， and increase in the co-localisation positivity rate and co-localised cell density of NCOA4 and LC3B （P＜0.05 or P＜0.01）. Compared with the model group， the ectopic endothelial tissue LC3BⅡ/LC3BⅠ values and the expression of NCOA4 and P-NF-κB proteins were down-regulated in the low- and high-dose Quyu Jiedu Formula group and mifepristone group， the colocalisation positivity rate of NCOA4 and LC3B significantly reduced， and the content of free iron and the level of IL-6 decreased （P＜0.05 or P＜0.01）. Compared with the mifepristone group， P62 more obvious up-regulated and TNF-α level reduced in the high-dose Quyu Jiedu Formula group （P＜0.05）. Compared with the low-dose Quyu Jiedu Formula group， the free iron content of ectopic tissues and the levels of IL-6 and TNF-α reduced in the high-dose Quyu Jiedu Formula group （P＜0.01）. ConclusionThe mechanism of endometriosis treatment by Quyu Jiedu Formula may be related to the inhibition of iron autophagy mediated by the NCOA4/NF-κB signalling pathway in endometriotic tissues， which improves endometrial inflammation.
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ObjectiveTo observe the effect of Youguiwan on the leptin/Janus kinase 2 （JAK2）/signal transducer and activator of transcription 3 （STAT3） signaling pathway in the lung tissue of the rat model of chronic obstructive pulmonary disease （COPD） due to kidney-Yang deficiency. MethodForty rats were modeled for COPD with the syndrome of kidney-Yang deficiency by intratracheal instillation of lipopolysaccharide on day 1 and day 14 and continuous fumigation for 6 weeks， during which hydrocortisone was injected intramuscularly at an interval of 3 days. The modeled rats were randomized into model， high- （11.7 g·kg-1）， medium- （5.85 g·kg-1）， and low-dose （2.93 g·kg-1） Youguiwan， and aminophylline （0.054 g·kg-1） group. In addition， 8 SD rats were set as the blank group. After the completion of modeling， the rats in each group were administrated with the corresponding drug by gavage for 28 consecutive days. After the last administration， samples were collected. A lung function analyzer was used to evaluate the lung function of rats. Enzyme-linked immunosorbent assay was employed to measure the levels of interleukin-17A （IL-17A）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in the bronchoalveolar lavage fluid （BALF）. Hematoxylin-eosin staining was employed to observe the pathological changes in the lung tissue， and Masson staining was employed to observe the deposition of blue collagen fibers around bronchi in the lung tissue and calculate the inflammation score. The immunofluorescence assay was employed to measure the protein content of collagen type Ⅰ （ColⅠ） and α-smooth muscle actin （α-SMA） in the bronchi. The protein and mRNA levels of leptin， IL-17A， JAK2， and STAT3 in the lung tissue were determined by Western blot and real-time fluorescence quantitative polymerase chain reaction， respectively. ResultCompared with the blank group， the model group showed decreased lung function （P<0.01）， elevated levels of IL-6， IL-17A， and TNF-α in the BALF （P<0.01）， and increased lung inflammation score， deposition of subcutaneous collagen fibers in the airway， and ColⅠ and α-SMA proteins （P<0.01）. Furthermore， the modeling up-regulated the proteins and mRNA levels of leptin， IL-17A， JAK2， and STAT3 in the lung tissue （P<0.01） and enhanced the phosphorylation of JAK2 and STAT3 （P<0.01）. Compared with the model group， high- and medium-dose Youguiwan improved the lung function， decreased the inflammation score， reduced collagen fiber deposition and ColⅠ and α-SMA proteins， lowered the levels of IL-6， IL-17A， and TNF-α in the BALF， down-regulated the mRNA and protein levels of leptin， JAK2， STAT3， and IL-17A， and weakened the phosphorylation of JAK2 and STAT3 （P<0.05， P<0.01）. The aminophylline group had higher IL-17A and TNF-α levels than the high-dose Youguiwan group， lower IL-17A level than the medium and low-dose Youguiwan groups， and lower TNF-α level than the low-dose Youguiwan group. Compared with the aminophylline group， the high- and medium-dose Youguiwan groups showed reduced deposition of collagen fibers and protein levels of ColⅠ and α-SMA around the bronchi in the lung tissue （P<0.05， P<0.01）， decreased inflammation score， and down-regulated protein and mRNA levels of leptin， JAK2， STAT3， and IL-17A in the lung tissue. ConclusionYouguiwan can prevent airway remodeling by inhibiting IL-17A to reduce inflammation and collagen deposition in COPD rats， which may be related to the inhibition of the leptin/JAK2/STAT3 signaling pathway.
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ObjectiveThe differential expression of microRNAs （miRNAs） between the active stage and the remission stage of ulcerative colitis （UC） was analyzed by bioinformatics method， and the regulatory relationship was constructed by screening the differentially expressed genes （DEGs）. The mechanism of Xizhuo Jiedu recipe in the treatment of UC was speculated and verified by animal experiments. MethodThe miRNAs data set of colonic mucosa tissue of UC patients was obtained from the gene expression database （GEO）， and the most differentially expressed miRNAs were screened by GEO2R， Excel， and other tools as research objects. TargetScan， miRTarbase， miRDB， STRING， TRRUST， and Matescape databases were used to screen key DEGs， predict downstream transcription factors （TFs）， gene ontology （GO）， and conduct Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis. The key signaling pathways were selected for animal experiments. In animal experiments， the UC mouse model was prepared by making the mouse freely drink 2.5% dextran sodium sulfate （DSS）. Xiezhu Jiedu recipe and mesalazine were given by gavage for seven days， and the inflammatory infiltration of colonic mucosa was observed by hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of miR-155-5p in colon tissue. Immunohistochemistry and Western blot were used to detect the protein expression levels of cytokine signal transduction inhibitor （SOCS1）， phosphorylated transcriptional signal transductor and activator 3 （p-STAT3）， phosphorylated Janus kinase 2 （p-JAK2）， and retinoic acid-associated orphan receptor-γt （ROR-γt）. The expression levels of transforming growth factor-β （TGF-β）， interleukin-17 （IL-17）， interleukin-6 （IL-6）， and interleukin-10 （IL-10） in serum were detected by enzyme linked immunosorbent assay （ELISA）. ResultThe GSE48957 dataset was screened from the GEO database， and miR-155-5p was selected as the research object from the samples in the active and remission stages. 131 DEGs were screened. The GO/KEGG enrichment analysis was closely related to biological processes such as positive regulation of miRNA transcription and protein phosphorylation， as well as signaling pathways such as stem cell signaling pathway， IL-17 signaling pathway， and helper T cell 17 （Th17） cell differentiation. The Matescape database was used to screen out 10 key DEGs， among which SOCS1 was one of the key DEGs of miR-155-5p. Further screening of the TFS of key DEGs revealed that STAT3 was one of the main TFs of SOCS1. The results of animal experiments showed that Xiezhu Jiedu Recipe could effectively down-regulate the mRNA expression of miR-155-5p and protein expression of p-STAT3， p-JAK2， and ROR-γt in colon tissue of UC mice and the expression of IL-17 and IL-6 in serum of UC mice， up-regulate the protein expression of SOCS1 and the expression of TGF-β and IL-10， increase the level of anti-inflammatory factors， and reduce inflammatory cell infiltration. ConclusionIt is speculated that Xizhuo Jiedu recipe may interfere with SOCS1 by regulating the expression of miR-155-5p in UC mice， inhibit the phosphorylation of STAT3， inhibit the differentiation of CD4+ T cells into Th17 cells， reduce the levels of pro-inflammatory factors （IL-17 and IL-6）， and increase the levels of anti-inflammatory factors （TGF-β and IL-10）. As a result， the inflammation of colon mucosa in UC mice was alleviated.
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Objective To investigate the risk factors of femoral head necrosis after internal fixation of fem-oral neck fracture,and to clarify the predictive role of serological index plasminogen activator inhibitors-1(PAI-1)on femoral head necrosis.Methods A total of 95 patients undergoing internal fixation for femoral neck fracture were included in the study.Relevant clinical information of patients was obtained and the serum PAI-1 levels of the patients before surgery,1,2,and 3 days after surgery were detected.After 1-year follow-up,patients were divided into necrosis group and non-necrosis group according to the occurrence of femoral head necrosis.Visual Analog Scale(VAS),Western Ontario McMaster University Osteoarthritis Index(WOMAC),and Harris Hip Score(HHS)were conducted in all patients one year after the surgery.The differences of basic clinical information and serum PAI-1 levels before and after the surgery between necrosis group and non-necrosis group were compared,and Logistic regression analysis was performed to identify the relevant risk factors for femoral head necrosis.The relationships between the PAI-1 level after operation and the VAS,WOMAC,and HHS scores of patients were figured out.The receiver operating characteristic(ROC)curve of serum PAI-1 as a predictive indicator for femoral head necrosis was drawn to clarify its predictive val-ue.Results Garden classification and reduction quality between the necrosis group and the non-necrosis group were risk factors for femoral head necrosis(P＜0.05).The serum PAI-1 at 1 day and 2 days after surgery in the necrosis group were significantly higher than that in the non-necrosis group(P＜0.05).The level of PAI-1 at 1 day and 2 days after surgery was positively correlated with VAS and WOMAC(P＜0.05),and negative-ly correlated with HHS(P＜0.05).Logistic regression analysis showed that the increase of serum PAI-1 level at 1 day and 2 days after surgery were risk factors for femoral head necrosis(P＜0.05).The ROC curve showed that serum PAI-1 level at 2 days after surgery had higher predictive value than that at 1 day after sur-gery,and the cut-off value was 44.8 ng/L,the sensitivity was 68.49％,the specificity was 86.36％,and the ar-ea under the curve(AUC)was 0.807.Conclusion The serum PAI-1 level at 1 day and 2 days after internal fixation of femoral neck fracture could be used to predict the occurrence of femoral head necrosis,especially the serum PAI-1 levels at 2 days after surgery.
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Objective To investigate the impact of ampelopsin(AMP)on oxygen glucose deprivation/reperfusion(OGD/R)induced neuronal damage and its mechanism,and to lay a foundation for the study of neonatal hypoxic-ischemic brain damage.Methods Neurons of newborn SD rats were isolated and cultured in vitro,and they were divided into 5 groups:control group(AMP 0 μmol/L),OGD/R group,low dose AMP group(OGD/R+AMP 20 μmol/L),high dose AMP group(OGD/R+AMP 30 μmol/L)and JAK2/STAT3 activator group(OGD/R+AMP 30 μmol/L+Coumermycin A1 10 μmol/L).CCK-8 method was used to de-tect the cell viability of different treatment groups,the lactate dehydrogenase(LDH)kit was used to detect the cell activity of LDH in the medium,flow cytometry was used to detect the apoptosis rate,enzyme-linked immunosorbent assay was used to detect the levels of interleukin-6(IL-6),interleukin-10(IL-10)and tumor necrosis factor α(TNF-α),the kit was used to detect the levels of reactive oxygen species(ROS),malondial-dehyde(MDA)and superoxide dismutase(SOD),and Western blotting was used to detect the expression of apoptosis related proteins B-cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax),enzymatic cleavage of cysteine containing aspartate protein hydrolase-3(C-caspase-3),tyrosine kinase 2(J AK2),phosphorylated JAK2(p-JAK2),signal transduction and transcription activating factor 3(STAT3)and phosphorylated STAT3(p-STAT3).Results Compared with the concentration of AMP of 0 μmol/L,the cell viability in con-centration of AMP of 5-30 μmol/L was not obvious different(P＞0.05),when the concentration of AMP was 40 μmol/L,the cell viability decreased obviously(P＜0.05).Compared with the control group,the cell viability,the levels of SOD fluorescence intensity,IL-10 and Bcl-2 in OGD/R group decreased obviously,the LDH activity,cell apoptosis rate,the levels of ROS,MDA,IL-6,TNF-α,Bax,C-caspase-3,p-JAK2/JAK2,and p-STAT3/STAT3 increased obviously(P＜0.05).Compared with OGD/R group,the cell viability,the levels of SOD fluorescence intensity,IL-10 and Bcl-2 in low and high dose AMP groups increased,the LDH activity,cell apoptosis rate,the levels of ROS,MDA,IL-6,TNF-α,Bax,C-caspase-3,p-JAK2/JAK2,and p-STAT3/STAT3 decreased(P＜0.05),and JAK2/STAT3 activator was able to reverse the protective effect of AMP on OGD/R induced neuronal.Conclusion AMP attenuates OGD/R induced neuronal by reducing oxidative stress and inflammatory response,and its mechanism may be related to inhibition of JAK2/STAT3 signal pathway phosphorylation.
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Objective To investigate the predictive value of tissue plasminogen activator(t-PA),chro-mogranin A(CgA),and lipoprotein related phospholipase A2(LP-PLA2)in serum for major adverse cardio-vascular event(MACE)after percutaneous coronary intervention(PCI).Methods A total of 120 patients with coronary heart disease who underwent PCI in the hospital from August 2020 to August 2022 were en-rolled in the study.According to whether MACE occurred within 1 year after PCI,the patients were divided into MACE group(33 cases)and non-MACE group(87 cases).The levels of serum t-PA,CgA,LP-PLA2 and clinical data were compared between the MACE group and the non-MACE group.Multivariate Logistic regres-sion was used to analyze the risk factors of MACE after PCI.Receiver operating characteristic(ROC)curve was used to analyze the predictive value of t-PA,CgA and LP-PLA2 alone or in combination for MACE after PCI.Results The proportion of patients with smoking history,NT-proBNP,CgA,LP-PLA2,and the propor-tion of patients with hypertension in the MACE group were higher than those in the non-MACE group(P＜0.05),while left ventricular ejection fraction(LVEF)and t-PA were lower than those in the non-MACE group(P＜0.05).There were no significant differences in age,gender composition,serum creatinine,triglyc-erides(TG),total cholesterol(TC),low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C),drinking history,NYHA cardiac function classification,combined diabetes,application of aspirin,and application of clopidogrel between the two groups(P＞0.05).Multivariate Logistic regression analysis showed that smoking history,increased NT-proBNP,hypertension,decreased LVEF,decreased t-PA,increased CgA and increased LP-PLA2 were risk factors for MACE after PCI(P＜0.05).ROC curve analysis showed that the areas under the curves(AUCs)of serum t-PA,CgA and LP-PLA2 alone or in combination for predicting MACE after PCI were 0.785(95％CI:0.693-0.877),0.678(95％CI:0.564-0.791),0.730(95％CI:0.636-0.824),0.888(95％CI:0.830-0.946),respectively.The efficacy of combined prediction was bet-ter than those of single detections(P＜0.05).Conclusion The lower the serum t-PA level is and the higher the CgA and LP-PLA2 levels are,the greater the risk of MACE after PCI is.The combination of the three in-dicators has higher value in predicting MACE after PCI.
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Objective To investigate the predictive value of serum interleukin(IL)-34 and soluble uroki-nase-type plasminogen activator receptor(suPAR)for poor prognosis in children with asthma.Methods A total of 184 children with asthma admitted to the hospital from January 2020 to December 2021 were enrolled in the study as the asthma group,and 184 healthy children who underwent physical examination in the hospital during the same period were enrolled as the healthy group.Enzyme-linked immunosorbent assay(ELISA)was used to measure the serum levels of IL-34 and suPAR in the two groups.The children in the asthma group were followed up for 1 year,and the prognosis was evaluated using the Asthma Control Test(ACT)score ta-ble.Logistic regression was used to analyze the influencing factors of poor prognosis in children with asthma.The receiver operating characteristic(ROC)curve was used to analyze the predictive value of serum IL-34 and suPAR levels for the prognosis of children with asthma.Results The asthma group had significantly higher serum levels of IL-34 and suPAR than the healthy group(P＜0.05).The incidence of poor prognosis was 22.65％(40/181).Compared with the good prognosis group,the poor prognosis group had significantly high-er proportion of children with preterm birth,passive smoking,a family history of asthma,a history of respira-tory infection,pet rearing,severe disease and serum levels of IL-34 and suPAR(P＜0.05),and a significantly lower proportion of children with breast feeding(P＜0.05).The multivariate Logistic regression analysis showed that preterm birth,family history of asthma,severe disease,and high levels of IL-34 and suPAR were risk factors for poor prognosis in children with asthma(P＜0.05),while breastfeeding was a protective factor(P＜0.05).The area under the ROC curve(AUC)of the combination of serum IL-34 and suPAR for predic-ting poor prognosis in children with asthma was 0.896(95％CI:0.842-0.936),which was greater than the AUC of IL-34 alone(Z=2.636,P=0.008)and the AUC of suPAR alone(Z=2.430,P=0.015).Conclusion Children with asthma have elevated serum levels of IL-34 and suPAR,both of which are risk fac-tors for poor prognosis in children with asthma.Both of them have a good predictive value for the prognosis of children with asthma,and the combination of the two has higher predictive efficiency.
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Objective To investigate the repair mechanism of baicalin on gastric mucosa of chronic atrophic gastritis mice based on the network pharmacology and animal experiments.Methods(1)Applied network pharmacology to predict and analyze the potential key targets of baicalin in the treatment of chronic atrophic gastritis.(2)Animal experiment:40 C57BL/6N mice were randomly divided into normal group,model group,Vitacoenzyme group and baicalin group,10 mice in each group.Except for the normal group,the other three groups of mice were treated with N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)by gavage combined with hunger and satiety disorder method to construct a chronic atrophic gastritis model.At the end of drug administration,the histopathological changes of gastric mucosa were observed by hematoxylin-eosin(HE)staining,the changes of gastrin(GAS)and prostaglandin E2(PGE2)levels in serum were detected by enzyme-linked immunosorbent assay(ELISA),and the mRNA and protein expression levels of Janus tyrosine kinase 1(JAK1),signal transducer and activator of transcription 3(STAT3)in the gastric mucosa were detected by real-time fluorescence quantitative polymerase chain reaction(qRT-PCR)and protein immunoblotting(Western Blot)methods,respectively.Results The results of network pharmacology showed that baicalin could spontaneously bind to the core targets JAK1 and STAT3.The results of animal experiments showed that compared with the normal group,the gastric mucosa of mice in the model group suffered from atrophy,disordered gland arrangement,the presence of a large number of lymphocytes,a significant increase in apoptotic index of the gastric mucosa(P＜0.05),a significant decrease in the levels of GAS and PGE2 in serum(P＜0.05),and a significant increase in the levels of mRNA and protein expressions of JAK1 and STAT3 in the gastric mucosa(P＜0.05);compared with the model group,the pathological changes of gastric mucosa in the Vitacoenzyme group and baicalin group were alleviated,the glands were arranged relatively neatly,the structure was more intact,the apoptosis index of gastric mucosal cells was significantly decreased(P＜0.05),the levels of GAS and PGE2 in serum were significantly increased(P＜0.05),and the mRNA and protein expression levels of JAK1 and STAT3 in gastric mucosa were significantly decreased(P＜0.05).There was no significant difference in the above-mentioned indexes between the baicalin group and the Vitacoenzyme group(P＞0.05).Conclusion Baicalin can effectively repair gastric mucosal lesions in mice with chronic atrophic gastritis,and its mechanism may be related to the down-regulation of mRNA and protein expressions of JAK1 and STAT3.
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Objective To investigate the therapeutic effects and mechanisms of Maxing Shigan Decoction on cough variant asthma(CVA)rats.Methods Sixty rats were randomly divided into normal group,model group,low and high dose groups of Maxing Shigan Decoction,and high-dose of Maxing Shigan Decoction + signal transducer and activator of transcription 3(STAT3)activator Colivelin(Col)group,12 rats in each group.Except for the normal group,the CVA model was constructed by intraperitoneal injection of ovalbumin combined with moxa fumigation in all other groups of rats.After the corresponding treatment,the rats were observed for signs and cough counts,airway resistance(RE)was detected by pulmonary function meter,eosinophils(EOS)were counted by Diff-Quik staining,histopathological features of the lungs and bronchial tubes were observed by hematoxylin-eosin(HE)staining method,and the lung tissues were detected by enzyme-linked immunosorbent assay(ELISA)for monocyte chemotactic protein 1(MCP-1),and tumor necrosis factor α(TNF-α),and the protein expression levels of interleukin 6(IL-6),STAT3,and transient receptor potential vanilloid-1 channel(TRPV1)were detected by Western Blot.Results Compared with the normal group,rats in the model group showed obvious asthma symptoms,severe inflammatory cell infiltration was seen in the lung tissue,bronchial epithelial cell necrosis,ciliated adhesion,mucus,and RE,EOS number,MCP-1 and TNF-α contents,and protein expression levels of IL-6,STAT3,TRPV1 were elevated(P＜0.05);compared with the model group,rats in the low-and high-dose groups of Maxing Shigan Decoction showed significant improvement in asthma symptoms,reduction in lung and bronchial injury,and dose-dependent reduction in RE,EOS number,MCP-1 and TNF-α contents,and protein expression levels of IL-6,STAT3,and TRPV1(P＜0.05);compared with the high-dose group of Maxing Shigan Decoction,the rats in the high-dose Maxing Shigan Decoction+Col group showed increased asthma,increased lung and bronchial injury,and increased RE,EOS number,MCP-1 and TNF-α contents,and protein expression levels of IL-6,STAT3,and TRPV1(P＜0.05).Conclusion Maxing Shigan Decoction can effectively improve cough variant asthma in rats,and its mechanism is related to the inhibition of IL-6/STAT3 signaling pathway and the high expression of TRPV1.
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Objective To investigate the role and regulatory mechanism of stress-inducing protein 1(SESN1)in liver gluconeogenesis of fasting mice.Methods RT-qPCR was used to detect mRNA expression of SESN1 in liver tissues of C57BL/6J mice and primary mouse hepatocytes treated with forskolin(Fsk)and dexamethasone(Dex).HepG2 cells were transfected with plasmids and the effects of SESN1 overexpression on mRNA expression of gluconeogenesis related genes PGC-1α,PEPCK and G6Pase was detected by RT-qPCR.The effect of SESN1 on the promoter activity of PGC-1α in HepG2 cells was studied using a dual luciferase reporter system.The effect of SESN1 on PGC-1α deacetylation was detected by overexpression of SESN1 and inhibition of SIRT1 expression.By knocking down SIRT1 expression,we detected whether it mediated the changes in mRNA levels of SESN1 in-duced gluconeogenesis related genes.Results The mRNA expression of SESN1 was significantly increased in liver tissues of starved C57BL/6J mice and in primary hepatocytes treated with Fsk and Dex(P<0.001).Over-expression of SESN1 in HepG2 cells promoted mRNA expression of PGC-1α,PEPCK and G6Pase(P<0.001)and promoter activity of PGC-1α(P<0.001).Over-expression of SESN1 decreased the acetylation level of PGC-1α in primary hepatocytes.Sirt family inhibitors NAM and shRNA adenovirus interfered with SIRT1 expression respective-ly,and antagonized the deacetylation effect of SESN1 on PGC-1α.The expression of PGC-1α,PEPCK and G6Pase induced by SIRT1 was also significantly impaired(P<0.000 1).Conclusions SESN1 regulates liver gluconeogene-sis in mice with a SIRT1-dependent mechanism.
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Objective To investigate the correlation between the expression of the activator of HSP90 ATPase-1(AHA1),lysyl oxidase like-2 protein(LOXL2)in osteosarcoma tissues with mRNA expression of invasion and metastasis genes and their clinical significance.Methods A total of 90 osteosarcoma patients diagnosed and treated in North China Medical and Health Group Fengfeng General Hospital from February 2016 to March 2017 were selected as the research object.The expression of AHA1 mRNA,LOXL2 mRNA and invasion and metastasis genes Wnt family member 9A(Wnt9a)mRNA,zinc finger E-box binding homologous box 1(ZEB1)mRNA,zinc finger E-box binding homologous box 1(ZEB2)mRNA,N-cadherin(N-cad)mRNA,and vimentin(Vim)mRNA in tissues were detected by real-time fluorescence quantitative PCR.Pearson correlation analysis was used for correlation analysis.The differences in expression of AHA1 mRNA and LOXL2 mRNA in osteosarcoma patients among different clinical characteristics were compared.Kaplan-Meier survival analysis was used to analyze the effect of AHA1 mRNA and LOXL2 mRNA on the prognosis of osteosarcoma patients.The prognostic factors of osteosarcoma patients were analyzed by univariate and multivariate COX regression.Results The expressions of AHA1 mRNA(3.16±0.59),LOXL2 mRNA(2.84±0.44)and invasion and metastasis genes[Wnt9a mRNA(3.23±0.42),ZEB1 mRNA(2.73±0.39),ZEB2 mRNA(2.52±0.56),N-cad mRNA(2.71±0.65)and Vim mRNA(2.81±0.73)]in osteosarcoma tissues were higher than those in paracancerous tissues(1.10±0.21,0.95±0.18,0.79±0.15,0.64±0.11,0.98±0.19,0.68±0.14,0.72±0.15),and the differences were statissically significant(t=31.206,37.716,51.903,48.931,24.706,28.964,26.605,all P<0.05).There was a significant positive correlation between AHA1 mRNA and LOXL2 mRNA expression in osteosarcoma(r=0.712,P<0.05).The expressions of AHA1 mRNA and LOXL2 mRNA were significantly positively correlated with the expressions of invasion and metastasis genes(Wnt9a,ZEB1,ZEB2,N-cad,and Vim mRNA)in tumor tissue of osteosarcoma group(r=0.504～0.720,all P<0.05).The expressions of AHA1 mRNA and LOXL2 mRNA in osteosarcoma tissues with Eneeking stage Ⅲ,soft tissue infiltration,and lung metastasis were higher than those in patients with Eneeking stage Ⅰ～Ⅱ,no soft tissue infiltration,and no lung metastasis,with significant differences(t=14.122～171.054,all P<0.05).The 5-year survival rates of patients in the AHA1 mRNA high expression group and low expression group were 36.36%(16/44)and 78.26%(36/46),respectively.The 5-year cumulative survival rate of patients in the AHA1 mRNA high expression group was significantly lower than that in the low expression group(Log-rank χ2=16.081,P<0.05).The 5-year survival rates of patients with high and low expression of LOXL2 mRNA were 34.88%(15/43)and 78.72%(37/47),respectively.The 5-year cumulative survival rate of patients in the LOXL2 mRNA high expression group was significantly lower than that in the low expression group(Log-rank χ2=15.880,P<0.05).Lung metastasis(OR=1.921,P<0.05),Eneeking stage Ⅲ(OR=1.906,P<0.05),AHA1 mRNA high expression(OR=1.405,P<0.05),and LOXL2 mRNA high expression(OR=1.733,P<0.05)were independent risk factors affecting the poor survival prognosis of osteosarcoma patients.Conclusion The expressions of AHA1 mRNA and LOXL2 mRNA in osteosarcoma were increased,and they were correlated with the expression of invasion and metastasis genes,indicating they may be independent risk factors affecting the poor survival and prognosis of osteosarcoma patients.
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ObjectiveTo investigate the mechanism of Baitouweng Tang in inhibiting the growth of esophageal cancer （EC） cells by regulating budding uninhibited by benzimidazoles 1 （BUB1）/signal transducer and activator of transcription 3 （STAT3） signaling pathway. MethodGene chip technology was used to explore the differential gene expression between esophageal cancer tissues and normal tissues and identified differentially expressed genes. The differentially expressed genes were analyzed by bioinformatics methods. EC cells were treated with 25， 50， 100， 200， 400， 800 mg·L-1 Baitouweng Tang. EC cell viability was detected by Thiazolyl Blue （MTT） colorimetry. Cell cycle and apoptosis were measured by flow cytometry. The expression of BUB1 was measured by real time quantitative polymerase chain reaction （Real-time PCR）. The protein levels of BUB1， STAT3， phosphorylated （p）-STAT3， Cyclin B1 （CCNB1）， cyclin-dependent kinase 1 （CDK1）， B-cell lymphoma-2 （Bcl-2）， cysteinyl aspartate-specific proteinase（Caspase）-3， and Caspase-9 were measured by Western blot. The migration and invasion abilities of the cells were measured by wound-healing and Transwell invasion assays. ResultDifferentially expressed genes were primarily involved in biological processes， signaling pathways， and network construction related to cell mitosis， with BUB1 identified as a key core gene. Compared with the control group， Baitouweng Tang inhibited BUB1 expression （P<0.05，P<0.01）. In vitro experiments showed that compared with the control group， Baitouweng Tang could significantly inhibit the growth （P<0.05，P<0.01）， migration and invasion （P<0.05，P<0.01） of EC cells， induce apoptosis （P<0.05，P<0.01）， and cause G2/M phase increase （P<0.01）. After treatment with Baitouweng Tang， compared with the results in the control group， the expression of Caspase-3， and Caspase-9 in EC cells increased significantly （P<0.05，P<0.01）， while the expression of Bcl-2， BUB1， CCNB1， and CDK1 decreased significantly （P<0.05，P<0.01）. Moreover， the STAT3 signaling pathway was also found to play an important role in this process. ConclusionBaitouweng Tang may inhibit the growth of EC cells by downregulating BUB1 and mediating the STAT3 signaling pathway.