Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 7 de 7
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Cancer Med ; 2020 Apr 02.
Artigo em Inglês | MEDLINE | ID: mdl-32239804

RESUMO

BACKGROUND: Non-small cell lung cancer (NSCLC) occupies the majority of lung cancer cases and is notorious for the awful prognosis. LIM domains-containing 1 (LIMD1) is suggested as a tumor suppressor in lung cancer, but its mechanism in NSCLC remains elusive. Present study aimed to uncover the mechanism of LIMD1 in NSCLC. METHODS: qRT-PCR was performed to analyze the level of LIMD1. The functions of LIMD1 in NSCLC cells were evaluated by CCK-8, EdU, and caspase-3 activity assays. RIP and pull-down assays were applied to determine the interaction of LIMD1 with heterogeneous nuclear ribonucleoprotein U (hnRNP U) and LIMD1-AS1. RESULTS: LIMD1 was downregulated in NSCLC samples and cells. Functionally, LIMD1 hindered proliferation and drove apoptosis in NSCLC cells. Moreover, long noncoding RNA (lncRNA) LIMD1 antisense RNA 1 (LIMD1-AS1) was downregulated in NSCLC samples and cell lines. LIMD1-AS1 knockdown abrogated NSCLC cell growth in vitro and in vivo. Mechanistically, LIMD1-AS1 stabilized LIMD1 mRNA through interacting with hnRNP U. Rescue experiments suggested that LIMD1-AS1 repressed NSCLC progression through LIMD1. CONCLUSIONS: LIMD1-AS1 suppressed NSCLC progression through stabilizing LIMD1 mRNA via hnRNP U, providing new thoughts for the improvement of molecular-targeted therapy for NSCLC.

2.
J Cardiovasc Pharmacol ; 74(5): 474-481, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31725080

RESUMO

Myocardial infarction (MI) is one of cardiovascular diseases with high incidence and mortality. MicroRNAs, as posttranscriptional regulators of genes, are involved in many diseases, including cardiovascular diseases. The aim of the present study was to determine whether miR-203 was functional in MI therapy and how it worked. Left anterior descending artery ligation and hypoxia/reoxygenation (H/R) treatment were, respectively, performed to obtain MI rats and hypoxia-injured H9c2 cells. Western blot and quantitative real-time polymerase chain reaction were used to determine protein levels and messenger RNA of relevant genes, respectively. Lentivirus-mediated overexpression of miR-203 was performed to study the miR-203 functions on left ventricular remodeling, infarct size, and cardiomyocyte apoptosis. Compared with the sham group, miR-203 levels were significantly decreased in MI and H/R groups. However, overexpressing miR-203 greatly improved the cardiac function, reduced infarct size in rats after MI and weakened infarction-induced apoptosis by increasing Bcl-2 and reducing decreasing Bax, cleaved caspase-3, and cleaved caspase-9. In addition, Protein tyrosine phosphatase 1B (PTP1B) was proved as a target of miR-203 in cardiomyocytes, and it was negatively regulated by miR-203. Further experiments indicated that PTP1B overexpression could remarkably inhibit miR-203-mediated antiapoptosis of cardiomyocytes and alleviate protective effects of miR-203 on mitochondria after H/R treatment. Altogether, miR-203 prevented infarction-induced apoptosis by regulating PTP1B, including reducing proapoptosis proteins, inactivating caspase pathway, and protecting mitochondria. In conclusion, miR-203 had abilities to alleviate MI-caused injury on myocardium tissues and reduce mitochondria-mediated apoptosis, which might be a potential target used for MI therapy.

3.
Artigo em Inglês | MEDLINE | ID: mdl-31425379

RESUMO

Myocardial infarction (MI) is one of cardiovascular diseases with high incidence and mortality. MicroRNAs (miRNAs), as post-transcriptional regulators of genes, are involved in many diseases, including cardiovascular diseases. The aim of present study was to determine whether miR-203 was functional in MI therapy and how it worked. Left anterior descending artery ligation and hypoxia/reoxygenation (H/R) treatment were respectively performed to obtain MI rats and hypoxia-injured H9c2 cells. Western blot and qRT-PCR were used to determine protein levels and mRNA of relevant genes, respectively. Lentivirus-mediated over-expression of miR-203 was performed to study the miR-203 functions on left ventricular remodeling, infarct size and cardiomyocyte apoptosis. Compared with the sham group, miR-203 levels were significantly decreased in MI and H/R groups. However, over-expressing miR-203 greatly improved the cardiac function, reduced infarct size in rats after MI, as well as weakened infarction-induced apoptosis by increasing Bcl-2 and reducing decreasing Bax, cleaved caspase-3 and cleaved caspase-9. In addition, PTP1B was proved as a target of miR-203 in cardiomyocytes, and it was negatively regulated by miR-203. Further experiments indicated that PTP1B over-expression could remarkably inhibit miR-203-mediated anti-apoptosis of cardiomyocytes, and alleviate protective effects of miR-203 on mitochondria after H/R treatment. Altogether, miR-203 prevented infarction-induced apoptosis by regulating PTP1B, including reducing pro-apoptosis proteins, inactivating caspase pathway and protecting mitochondria. In conclusion, miR-203 had abilities to alleviate MI-caused injury on myocardium tissues and reduce mitochondria-mediated apoptosis, which might be a potential target used for MI therapy.

4.
Medicine (Baltimore) ; 98(32): e16462, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31393350

RESUMO

The outcome of patients with acute type B aortic dissection (BAAD) is largely dictated by whether or not the case is "complicated." The purpose of this study was to investigate the risk factors leading to in-hospital death among patients with BAAD and then to develop a predictive model to estimate individual risk of in-hospital death.A total of 188 patients with BAAD were enrolled. Risk factors for in-hospital death were investigated with univariate and multivariable logistic regression analysis. Significant risk factors were used to develop a predictive model.The in-hospital mortality rate was 9% (17 of 188 patients). Univariate analysis revealed 7 risk factors to be statistically significant predictors of in-hospital death (P < .1). In multivariable analysis, the following variables at admission were independently associated with increased in-hospital mortality: hypotension (odds ratio [OR], 4.85; 95% confidence interval [CI], 1.12-18.90; P = .04), ischemic complications (OR, 8.24; 95% CI, 1.25-33.85; P < .001), renal dysfunction (OR, 12.32; 95% CI, 10.63-76.66; P < .001), and neutrophil percentage ≥80% (OR, 5.76; 95% CI, 2.58-12.56; P = .03). Based on these multivariable results, a reliable and simple prediction model was developed, a total score of 4 offered the best point value.Independent risk factors associated with in-hospital death can be predicted in BAAD patients. The prediction model could be used to identify the prognosis for BAAD patients and assist physicians in their choice of management.


Assuntos
Aneurisma Dissecante/mortalidade , Aneurisma da Aorta Torácica/mortalidade , Mortalidade Hospitalar , Adulto , Idoso , Aneurisma Dissecante/classificação , Aneurisma Dissecante/terapia , Aneurisma da Aorta Torácica/classificação , Aneurisma da Aorta Torácica/terapia , Comorbidade , Feminino , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Neutrófilos/metabolismo , Razão de Chances , Fatores de Risco
5.
Ecotoxicol Environ Saf ; 179: 249-256, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31054378

RESUMO

The functional role of 1,25-vitamin D3 in cooking oil fumes (COFs)-derived PM2.5-induced cell damage is largely unexplored. The present study investigated the protective role of 1,25-vitamin D3 against cell injury by possible involvement of JAK/STAT and NF-κB signaling pathways in cardiomyocytes. Cell viability was measured using CCK-8 assay, and cell apoptosis was analyzed by flow cytometry, qRT-PCR and Western blot in cultured rat neonatal cardiomyocytes treated with 1,25-vitamin D3 and COFs-derived PM2.5. Expressions of JAK/STAT and NF-κB signaling pathway were measured by Western blot. The results suggested that treatment with COFs-derived PM2.5 significantly decreased cell viability and increased apoptosis and oxidative stress in cultured rat neonatal cardiomyocytes. 1,25-vitamin D3 pretreatment alleviated the cell injury by increasing cell viability and decreasing apoptosis in the cardiomyocytes. 1,25-vitamin D3 pretreatment also decreased the ROS level and inflammation in the cardiomyocytes. Furthermore, 1,25-vitamin D3 pretreatment alleviated COFs-derived PM2.5-evoked elevation of JAK/STAT and NF-κB signaling pathways. Our study showed that 1,25-vitamin D3 pretreatment protected cardiomyocytes from COFs-derived PM2.5-induced injury by decreasing ROS, apoptosis and inflammation level via activations of the JAK/STAT and NF-κB signaling pathways.


Assuntos
Poluentes Atmosféricos/toxicidade , Anti-Inflamatórios/farmacologia , Colecalciferol/farmacologia , Miócitos Cardíacos/efeitos dos fármacos , Material Particulado/toxicidade , Animais , Apoptose/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Culinária/métodos , Miócitos Cardíacos/metabolismo , NF-kappa B/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Tamanho da Partícula , Ratos , Transdução de Sinais/efeitos dos fármacos
6.
Medicine (Baltimore) ; 96(17): e6647, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28445265

RESUMO

Diabetes mellitus (DM) has been proved to be a predictor of adverse outcomes after percutaneous coronary intervention (PCI). Drug-eluting stents (DESs) could reduce the adverse events in DM patients. In this study, we aimed to analyze the clinical outcome after DES implantation in diabetic versus nondiabetic patients in China. Totally, 200 Chinese DM patients and 400 Chinese non-DM patients were enrolled in this retrospective study. Compared with non-DM patients, DM patients were more likely to have a higher incidence of cardiac death (3.5% vs. 1.0%, P = .048), stent thrombosis (2.5% vs. 0.5%, P = .044), target lesion revascularization (6.0% vs. 1.8%, P = .005), target vessel failure (15.5% vs. 8.0%, P < .001), target lesion failure (14.0% vs. 4.3%, P < .001), myocardial infarction (4.5% vs. 1.5%, P = .030), and major adverse cardiac events (12.5% vs. 5.0%, P = .001) at 2-year follow-up. However, the incidence of target vessel revascularization (7.5% vs. 5.5%, P = .340) was similar between DB and non-DB patients. Patients with DB (hazard ratio [HR] = 2.54, P = .001), older than 80 years (HR = 1.33, P = .027) with hypercholesterolemia (HR = 1.03, P < .001), serum creatinine >177 µmol/L (HR = 3.04, P = .011), a history of cerebral vascular accident (HR = 4.29, P = .010), or a history of myocardial infarction (HR = 31.4, P < .001) were more likely to experience adverse events. In China, DM could also be served as an independent predictor of adverse outcomes after DES implantation. These patients should be reexamined more frequently.


Assuntos
Síndrome Coronariana Aguda/tratamento farmacológico , Síndrome Coronariana Aguda/cirurgia , Doença da Artéria Coronariana/tratamento farmacológico , Doença da Artéria Coronariana/cirurgia , Complicações do Diabetes , Stents Farmacológicos/efeitos adversos , Síndrome Coronariana Aguda/complicações , Síndrome Coronariana Aguda/mortalidade , Idoso , China , Doença Crônica , Doença da Artéria Coronariana/complicações , Doença da Artéria Coronariana/mortalidade , Feminino , Seguimentos , Humanos , Masculino , Intervenção Coronária Percutânea/efeitos adversos , Estudos Retrospectivos , Resultado do Tratamento
7.
Anatol J Cardiol ; 15(6): 496-501, 2015 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-25550177

RESUMO

OBJECTIVE: Dysfunction of cardiac autonomic nerve system is considered as one of risk factors for coronary atherosclerotic heart disease. Heart rate variability (HRV) has been used to study the correlation between damage of coronary artery and dysfunction of autonomic nervous system. We hypothesize the correlation between damage of coronary artery and dysfunction of autonomic nervous system by HRV among subjects with stable angina. METHODS: A 236 subjects who diagnosed as stable angina pectoris by elective coronary angiography, were divided into two groups by Gensini score system (GS):GS≤32 (GS1) and GS2>32 (GS2). Subgroups were divided based on location of stenosis lesions and the number of coronary artery disease. 86 subjects suspicious with stable angina pectoris with normal coronary angiography were selected as the control group. All subjects were received 24-hour ambulatory electrocardiogram and the result of time-domain HRV was analyzed (SDNN, SDANN, SDNNind, RMSSD, PNN50). RESULTS: Compared with control group, SDNN, SDNNind and RMSSD lower in GS1, and SDNN, SDANN, SDNNind, RMSSD, PNN50 lower in GS2; ccompared with GS1, SDNN was lower in GS2. Compared with control group, SDNN in one-vessel, SDNN, SDANN in two-vessel diseased and in three-vessel diseased were lower, and compared with two-vessel diseased, SDNN, SDANN lower in three-vessel diseased. Compared with right-coronary artery diseased, SDNN and SDANN in left-coronary artery diseased group were lower, while compared with lesions in left circumflex, SDNN in lesions in left anterior descending artery lower. CONCLUSION: HRV may be play a crucial role in estimating the correlation between damage of coronary artery and dysfunction of autonomic nerve system.


Assuntos
Angina Pectoris/fisiopatologia , Arritmias Cardíacas/fisiopatologia , Doença da Artéria Coronariana/fisiopatologia , Frequência Cardíaca , Sistema Nervoso Autônomo , Angiografia Coronária , Doença da Artéria Coronariana/diagnóstico por imagem , Eletrocardiografia , Eletrocardiografia Ambulatorial , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Índice de Gravidade de Doença
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA