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1.
Br J Anaesth ; 125(3): 282-290, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32536445

RESUMO

BACKGROUND: Postoperative neurocognitive disorders may arise in part from adverse effects of general anaesthetics on the CNS, especially in older patients or individuals otherwise vulnerable to neurotoxicity because of systemic disease or the presence of pre-existing neuropathology. Previous studies have documented cytokine and injury biomarker responses to surgical procedures that included general anaesthesia, but it is not clear to what degree anaesthetics contribute to these responses. METHODS: We performed a prospective cohort study of 59 healthy volunteers aged 40-80 yr who did not undergo surgery. Plasma markers of neurological injury and inflammation were measured immediately before and 5 h after induction of general anaesthesia with 1 minimum alveolar concentration of sevoflurane. Biomarkers included interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α), C-reactive protein (CRP), and neural injury (tau, neurofilament light [NF-L], and glial fibrillary acidic protein [GFAP]). RESULTS: Baseline biomarkers were in the normal range, although NF-L and GFAP were elevated as a function of age. At 5 h after induction of anaesthesia, plasma tau, NF-L, and GFAP were significantly decreased relative to baseline. Plasma IL-6 was significantly increased after anaesthesia, but by a biologically insignificant degree (<1 pg ml-1); plasma TNF-α and CRP were unchanged. CONCLUSIONS: Sevoflurane general anaesthesia without surgery, even in older adults, did not provoke an inflammatory state or neuronal injury at a concentration that is detectable by an acute elevation of measured plasma biomarkers in the early hours after exposure. CLINICAL TRIAL REGISTRATION: NCT02275026.


Assuntos
Anestesia Geral/métodos , Anestésicos Inalatórios/sangue , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Proteína C-Reativa/efeitos dos fármacos , Estudos de Coortes , Feminino , Proteína Glial Fibrilar Ácida/sangue , Proteína Glial Fibrilar Ácida/efeitos dos fármacos , Voluntários Saudáveis , Humanos , Interleucina-6/sangue , Masculino , Pessoa de Meia-Idade , Proteínas de Neurofilamentos/sangue , Proteínas de Neurofilamentos/efeitos dos fármacos , Estudos Prospectivos , Valores de Referência , Fator de Necrose Tumoral alfa/sangue , Fator de Necrose Tumoral alfa/efeitos dos fármacos
2.
Arch. Clin. Psychiatry (Impr.) ; 47(1): 7-12, Jan.-Feb. 2020. tab, graf
Artigo em Inglês | LILACS | ID: biblio-1088740

RESUMO

Abstract Objectives This study aimed to explore the effect of antidepressant treatment on the HPA axis, changes in depression score, and serum levels of TNF-α in depressed infertile women. Methods In this randomized controlled trial research, 60 infertile women who had undergone in vitro fertilization (IVF) treatment with depression scores between 16-47 were divided into two groups. The intervention group with fluoxetine capsule was under treatment for two months before the embryo transfer, while the control group was given placebo. Depression score, serum levels of tumor necrosis factor alpha (TNF-α) as well as cortisol hormone levels were measured and recorded both before and after the intervention. The data were analyzed using SPSS version 21 software. Results We analyzed the data related to 55 subjects who had undergone embryo transfer. 7 subjects in the intervention group and 3 in the control group got pregnant. We observed a significant decrease in the depression score (p < 0/001) and serum levels of cortisol (p = 0/001) in the intervention group. There was a significant increase in the serum levels of TNF-α in the intervention group (p < 0/001). There was a significant difference between the two groups in the number of pregnancies (p = 0.04). However, there was no statistical difference between them with regard to the number of harvested oocytes (p = 0.174). Discussion Decrease in depression score and cortisol level, and an increase in the levels of TNF-α in the intervention group caused any changes in the number of oocytes in comparison with the control group. However, the number of pregnancies was larger in the intervention group.


Assuntos
Humanos , Feminino , Adulto , Fator de Necrose Tumoral alfa/sangue , Depressão/tratamento farmacológico , Sistema Hipotálamo-Hipofisário/efeitos dos fármacos , Infertilidade Feminina/psicologia , Placebos/uso terapêutico , Escalas de Graduação Psiquiátrica , Psicometria/métodos , Gravidez/psicologia , Hidrocortisona/sangue , Fertilização In Vitro , Aborto Espontâneo/etiologia , Fluoxetina/uso terapêutico , Inquéritos e Questionários , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Resultado do Tratamento , Depressão/complicações , Depressão/diagnóstico , Infertilidade/etiologia
3.
Nat Prod Res ; 34(2): 225-232, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30580619

RESUMO

One new aryldihydronaphthalene-type lignan (1) together with eight known lignans (2-4, 7-11) as well as two caffeic-acid dimers (5, 6) were isolated from an ethanol extract of the whole plant of Corispermum mongolicum Iljin (Chenopodiaceae). The chemical structures of these compounds were determined from 1D and 2D NMR and HR-ESI-MS spectra, and results were compared with data from the literature. This study is the first demonstration of nine compounds (2 and 4-11) isolated from the Chenopodiaceae family, with one of these (3) from the genus Corispermum. Anti-inflammatory effects of the isolated compounds were evaluated in terms of inhibition of production of nitric oxide, tumour necrosis factor-α, and interleukin-6 in lipopolysaccharide-induced RAW 264.7 cells.


Assuntos
Anti-Inflamatórios/isolamento & purificação , Chenopodiaceae/química , Lignanas/isolamento & purificação , Extratos Vegetais/química , Animais , Anti-Inflamatórios/química , Anti-Inflamatórios/farmacologia , Chenopodiaceae/metabolismo , Interleucina-6/biossíntese , Lignanas/química , Lignanas/farmacologia , Lipopolissacarídeos , Camundongos , Estrutura Molecular , Óxido Nítrico/antagonistas & inibidores , Óxido Nítrico/biossíntese , Células RAW 264.7 , Fator de Necrose Tumoral alfa/biossíntese , Fator de Necrose Tumoral alfa/efeitos dos fármacos
4.
Rev. esp. enferm. dig ; 111(11): 823-827, nov. 2019. ilus, tab, graf
Artigo em Inglês | IBECS | ID: ibc-190504

RESUMO

Background and aims: to investigate the potential effect and mechanism of Salvia miltiorrhiza in Gynura segetum-induced hepatic sinusoidal obstruction syndrome (HSOS). Methods: the mice were gavaged with PBS, Gynura segetum or Gynura segetum, along with 100 or 200 mg/kg Salvia miltiorrhiza. Histological scoring and liver function were performed. The expression of tumor necrosis factor-alpha (TNF-alfa), vascular cellular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and nuclear transcription factor P65 (NF-κBp65) were determined by reverse transcriptase polymerase chain reaction (RT-PCR) and western blot. Results: liver function were effectively improved in the Salvia miltiorrhiza groups. The levels of TNF-alfa, VCAM-1, ICAM-1 and NF-κBp65 were significantly lower in the Salvia miltiorrhiza groups than in the Gynura segetum group. Conclusions: Salvia miltiorrhiza has a therapeutic effect on Gynura segetum-induced HSOS


No disponible


Assuntos
Animais , Ratos , Salvia miltiorrhiza , Extratos Vegetais/farmacocinética , Hepatopatia Veno-Oclusiva/tratamento farmacológico , Moléculas de Adesão Celular/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Molécula 1 de Adesão de Célula Vascular/efeitos dos fármacos , Fator de Transcrição RelA/efeitos dos fármacos , Modelos Animais de Doenças , Hepatopatia Veno-Oclusiva/induzido quimicamente , Testes de Função Hepática/métodos , Substâncias Protetoras/análise
5.
Am J Physiol Endocrinol Metab ; 317(6): E1205-E1217, 2019 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-31573846

RESUMO

Interleukin-8 (IL-8, also named CXCL8) binds to its receptors (CXCR1 and CXCR2) with subsequent recruitment of neutrophils and enhancement of their infiltration into inflamed sites, which exaggerates inflammation in many diseases. Recent studies have proposed that metabolic disorders can be attenuated by counteracting certain inflammatory signal pathways. In this study, we examined whether intervention with G31P, an antagonist of CXCL8, could attenuate tissue inflammation and development of metabolic disorders in db/db mice. The db/m and db/db mice were subcutaneously injected with G31P or equivalent normal saline once a day for 6 wk. The physical and metabolic parameters, glucose tolerance, insulin sensitivity, hepatic lipid accumulation, and inflammation markers were measured. G31P improved hepatic insulin sensitivity by modulating expression of genes related to gluconeogenesis and phosphorylated Akt levels. The expressions of several genes encoding proteins involved in de novo lipogenesis were decreased in G31P-treated db/db mice. Meanwhile, immune cell infiltration and cytokine release were attenuated in db/db mice with G31P treatment. G31P also improved the ratio of proinflammatory M1 and anti-inflammatory M2 macrophages. Furthermore, G31P ameliorates metabolic disturbances via inhibition of CXCR1 and CXCR2 pathways in db/db mice. These data suggest that the selective inhibition of CXC chemokines may have therapeutic effects on symptoms associated with obesity and diabetes.


Assuntos
Diabetes Mellitus Tipo 2/metabolismo , Resistência à Insulina , Interleucina-8/antagonistas & inibidores , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fragmentos de Peptídeos/farmacologia , Receptores de Interleucina-8A/antagonistas & inibidores , Receptores de Interleucina-8B/antagonistas & inibidores , Animais , Citocinas/efeitos dos fármacos , Citocinas/metabolismo , Diabetes Mellitus Tipo 2/genética , Modelos Animais de Doenças , Ácidos Graxos não Esterificados/metabolismo , Gluconeogênese/efeitos dos fármacos , Gluconeogênese/genética , Insulina/metabolismo , Interleucina-6/metabolismo , Interleucina-8/genética , Interleucina-8/metabolismo , Fígado/metabolismo , Fígado/patologia , Macrófagos/efeitos dos fármacos , Camundongos , Fosforilação , Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptores de Interleucina-8A/genética , Receptores de Interleucina-8A/metabolismo , Receptores de Interleucina-8B/genética , Receptores de Interleucina-8B/metabolismo , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo
6.
Medicine (Baltimore) ; 98(40): e17126, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31577702

RESUMO

BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) synthesis by human periodontal ligament fibroblast cells (hPDLFs). In addition, we aimed to determine the involvement of the nuclear factor-kappa B (NF-κB) pathway in any changes in IL-1ß and TNF-α expression observed in response to LPS and NAC. METHODS: HPDLFs were obtained by primary culture. The culture medium used in this experiment was Dulbecco's Modified Eagle Medium (DMEM low-glucose). Cells were stimulated with various concentrations of NAC or LPS. Cell proliferation was measured at various time-points with the cell Counting Kit 8 (CCK-8) assay. mRNA levels of IL-1ß and TNF-α were determined by real-time quantitative polymerase chain reaction (RT-qPCR) analysis. Protein levels of IL-1ß and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA). Protein and mRNA expression levels of NF-κB were measured by western blot and RT-qPCR. RESULTS: The results showed that LPS treatment in hPDLFs induced mRNA and protein expression of IL-1ß, TNF-α, and NF-κB. However, these effects were eliminated by pretreatment with NAC. Pretreatment with both NAC (1 mmol/L) and BAY11-7082 (10 µmol/L) significantly inhibited the NF-κB activity induced by LPS. CONCLUSION: NAC inhibits the LPS-mediated synthesis of tumor TNF-α and IL-1ß in hPDLFs, through the NF-κB pathway.


Assuntos
Acetilcisteína/farmacologia , Fibroblastos/efeitos dos fármacos , Interleucina-1beta/efeitos dos fármacos , NF-kappa B/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Células Cultivadas , Ensaio de Imunoadsorção Enzimática , Fibroblastos/metabolismo , Humanos , Interleucina-1beta/biossíntese , Lipopolissacarídeos/farmacologia , NF-kappa B/metabolismo , Ligamento Periodontal , RNA Mensageiro/metabolismo , Reação em Cadeia da Polimerase em Tempo Real , Transdução de Sinais/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo
7.
Medicine (Baltimore) ; 98(39): e17285, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31574846

RESUMO

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha), among cytokines that mediate the inflammatory process, plays an important role in diseases involving the loss of intestinal barrier integrity. Several molecules with anti-TNF-alpha activity have been studied aiming to develop new therapies. The purpose of this paper is to describe the systematic review protocol of experimental studies that determine mechanisms of action of molecules with anti-TNF-alpha activity on intestinal barrier inflammation. METHODS: This protocol is guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes Protocols (PRISMA-P). The databases to be searched are PubMed, EMBASE, Scopus, ScienceDirect, and Web of Science. Experimental studies in rats or mice that assessed the activity of anti-TNF-alpha molecules in models of intestinal barrier inflammation will be included in the systematic review. Studies characteristics, experimental model, and main results will be described and the bias risk assessment will be performed. Two independent reviewers will perform study selection, data extraction, and methodological quality assessment. A narrative synthesis will be made for the included studies. Also, if sufficient data is available, a meta-analysis will be conducted. I statistics will be used to assess heterogeneity. RESULTS: The present protocol will assist in producing a systematic review that identifies the mechanisms underlying the reduction of TNF-alpha in intestinal barrier inflammation models. CONCLUSION: The systematic review may contribute to the theoretical basis of research on new molecules with anti-TNF-alpha potential and, consequently, in the development of new therapies employed in humans. PROSPERO REGISTRATION NUMBER: CRD42019131862.


Assuntos
Fármacos Gastrointestinais/farmacologia , Mucosa Intestinal/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Animais , Humanos , Inflamação , Projetos de Pesquisa , Revisões Sistemáticas como Assunto , Fator de Necrose Tumoral alfa/antagonistas & inibidores
8.
Biol Res ; 52(1): 49, 2019 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-31492195

RESUMO

BACKGROUND: Psoriasis is a common and intractable skin disease affecting the physical and mental health of patients. The accumulation of ROS is involved in the pathogenesis of psoriasis and antioxidants are believed to be therapeutic. This study aimed to investigate the therapeutic efficacy of astilbin on ROS accumulation in psoriasis. RESULTS: The study showed that 50 µg/ml astilbin could inhibit the growth and reduce the accumulation of ROS in HaCaT cells stimulated by IL-17 and TNF-α. Astilbin could elevate the Nrf2 accumulation in the nuclei, eventually leading to the transcriptional activation of various antioxidant proteins and reducing the expression of VEGF. CONCLUSIONS: Our results collectively suggest that astilbin could induce Nrf2 nucleus translocation, which is contribute to reduce the ROS accumulation and VEGF expression, and inhibit the proliferation of HaCaT cells.


Assuntos
Flavonóis/administração & dosagem , Queratinócitos/efeitos dos fármacos , Fator 2 Relacionado a NF-E2/efeitos dos fármacos , Psoríase/tratamento farmacológico , Espécies Reativas de Oxigênio/metabolismo , Fator A de Crescimento do Endotélio Vascular/efeitos dos fármacos , Animais , Modelos Animais de Doenças , Interleucina-17/metabolismo , Queratinócitos/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Fator 2 Relacionado a NF-E2/metabolismo , Psoríase/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo
9.
Arch Oral Biol ; 108: 104519, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31470142

RESUMO

Periodontitis is the most common oral disease which can destroy periodontal supporting tissue leading to tooth loss. Anti-inflammatory substances can effectively improve periodontitis. The present study was to explore whether Coronarin D could resolve the periodontal inflammation and improve the proliferation and osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs). After treatment with TNF-α or Coronarin D, CCK-8 assay was used to detect the viability of hPDLSCs. Alkaline phosphatase (ALP) activity kit and alizarin red staining were used to determine the ALP activity and mineralization osteogenesis ability of hPDLSCs. The cell cycle proteins (CDK2, cyclinE1, P27), differentiation-related proteins (Oct4, Sox2, Runx2) and anti-inflammatory signaling proteins (TNF-a, NF/KBp50) were detected by western blot. The results demonstrated that Coronarin D could improve the viability, proliferation, differentiation and mineralization osteogenesis of hPDLSCs induced by TNF-α. And, expression of cell cycle proteins (CDK2, cyclinE1, P27), differentiation-related proteins (Oct4, Sox2, Runx2) and anti-inflammatory signaling proteins (TNF-a, NF/KBp50) were changed after the TNF-α induced hPDLSCs treated with Coronarin D. In conclusion, the presented data indicated that Coronarin D could improve the TNF-α induced proliferation and osteogenic differentiation of human periodontal ligament stem cells.


Assuntos
Diferenciação Celular , Diterpenos , Osteogênese , Ligamento Periodontal , Fator de Necrose Tumoral alfa , Proliferação de Células , Células Cultivadas , Diterpenos/farmacologia , Humanos , Ligamento Periodontal/metabolismo , Células-Tronco , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo
10.
Nutr J ; 18(1): 39, 2019 07 19.
Artigo em Inglês | MEDLINE | ID: mdl-31324181

RESUMO

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide. Evidence showed that anthocyanins might have effects on NAFLD. Protective effects of Cornelian cherry (Cornus mas L.) extract, as an anthocyanins-rich source, on liver were reported in animal studies. However, very few clinical trials were conducted in this regard. Thus, the aim of this research will be to evaluate the effect of supplementation with total anthocyanin-base standardized cornelian cherry fruit extract on liver function (Serum levels of Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), cytokeratin-18 fragment M30 (CK-18 M30), as well as steatosis and fibrosis of liver), tumor necrosis factor α (TNF-α), malondealdehyde (MDA), and adiponectin in patients with NAFLD. METHODS: In a double-blind randomized clinical trial, 80 NAFLD patients will be studied. The patients will be randomly assigned into two groups. The intervention group will receive the cornelian cherry extract, containing 320 mg.d- 1 anthocyanins, per day for 12 weeks. The control group will also take the placebo daily for 12 weeks. Liver function (Serum levels of AST, ALT and CK-18 M30; steatosis and fibrosis of liver), serum levels of TNF-α, MDA, and adiponectin will be measured at the baseline and the end of trial for both groups and their results will be compared. DISCUSSION: Considering evidences about the useful impacts of anthocyanins on NAFLD, the effects of supplementation with cornelian cherry extract will be investigated on the important variables related to NAFLD. TRIAL REGISTRATION: Iranian Registry of Clinical Trials ( IRCT20180419039359N1 ).


Assuntos
Adiponectina/sangue , Antocianinas/farmacologia , Cornus , Fígado/efeitos dos fármacos , Malondialdeído/sangue , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Extratos Vegetais/farmacologia , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Adulto , Idoso , Método Duplo-Cego , Feminino , Humanos , Fígado/fisiopatologia , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/sangue , Projetos de Pesquisa , Fator de Necrose Tumoral alfa/sangue
11.
Phytother Res ; 33(9): 2401-2408, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31317585

RESUMO

Lupus nephritis (LN) is an autoimmune disease caused by systemic lupus erythematosus. Excessive proliferation of mesangial cells is one of the most serious pathological manifestations of LN. In addition, the expression of PTX3 is elevated in the serum of patients with LN. Quercetin has good anti-inflammatory effects and immunomodulatory activities. In this study, the result of MTT indicated that quercetin treatment alleviated the excessive proliferation of mesangial cells. ELISA and immunofluorescence experiments showed that quercetin treatment inhibited the expression of PTX3. Three doses of quercetin (20, 40, and 80 µM) were selected for the experiment. It is noteworthy that the efficacy of quercetin at 80 µM was significantly better than that of other dose groups. And the effect in inhibiting PTX3 expression was comparable with that of the PDTC (80 µM) positive control. Western blot and qRT-PCR analysis revealed that quercetin treatment reduced the expression of nuclear factor-κB p65 and IKKß, increased the expression of IκBα, and inhibited the expression of PTX3. In conclusion, through inhibiting the activation of nuclear factor-κB signaling pathway, quercetin treatment could reduce the expression of PTX3 and inhibit the excessive proliferation of mesangial cells, suggesting that quercetin is a potential therapeutic drug for LN.


Assuntos
Antioxidantes/uso terapêutico , Proteína C-Reativa/efeitos dos fármacos , NF-kappa B/metabolismo , Quercetina/uso terapêutico , Componente Amiloide P Sérico/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Antioxidantes/farmacologia , Proliferação de Células , Humanos , Quercetina/farmacologia , Transdução de Sinais , Fator de Necrose Tumoral alfa/metabolismo
12.
Zhonghua Liu Xing Bing Xue Za Zhi ; 40(6): 682-685, 2019 Jun 10.
Artigo em Chinês | MEDLINE | ID: mdl-31238619

RESUMO

Objective: To explore the effect of lipopolysaccharide intervention program on Legionella pneumonia. Methods: C3H/HeN mice (6-8 weeks old) were used as experimental animals. The mice were randomly divided into lipopolysaccharide intervention, non-lipopolysaccharide intervention and control groups. Each group was again divided into three time points: 12 h, 24 h and 48 h. Mice in the lipopolysaccharide intervention group were intraperitoneally injected with E. coli lipopolysaccharide (100 ng per mice), and the rest groups were intraperitoneally injected with normal saline. After 24 hours, mice in the lipopolysaccharide intervention and the non-intervention groups mice were infected with Legionella by tracheal injection and the control group was given the same amount of saline. All the mice were killed at 12, 24 and 48 hours respectively. The mice were anatomized, lungs of the mice were separated and weighed. Organ coefficients (lung weight/body weight of mice) were calculated. 1 ml Orbital blood was collected. Toll-like receptor 4 (TLR4) levels of peripheral blood mononuclear cells were measured by flow cytometry. The contents of TNF-α and IL-1ß in the upper left lung lobe were measured by ELISA. Results: In the lung organs, the coefficients of lipopolysaccharide non-intervention group were higher than the other groups and there was no significant difference seen between the lipopolysaccharide intervention group and the controls. TLR4 peaked at 12 hours in both the lipopolysaccharide intervention and the non-intervention groups while the TLR4 level in the intervention group was higher than that in the non-intervention group. There were no significant differences appeared on the TLR4 expression levels between the two Legionella pneumonia modelled groups at 24 or 48 hours. There was no significant difference seen regarding the concentration of TNF-α and IL-1ß between the intervention and the control groups. The secretion levels of TNF-α and IL-1ß in the non-intervention group were higher than those in the intervention group at each time point. Conclusion: The lipopolysaccharide intervention program may alleviate the inflammatory symptoms of Legionella infection.


Assuntos
Legionella , Lipopolissacarídeos/farmacologia , Pneumonia , Receptor 4 Toll-Like/metabolismo , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Experimentação Animal , Animais , Escherichia coli , Leucócitos Mononucleares , Lipopolissacarídeos/administração & dosagem , Camundongos , Camundongos Endogâmicos C3H , Distribuição Aleatória
13.
Nan Fang Yi Ke Da Xue Xue Bao ; 39(5): 598-602, 2019 May 30.
Artigo em Chinês | MEDLINE | ID: mdl-31140426

RESUMO

OBJECTIVE: To investigate the protective effect of quercetin against lipopolysaccharide (LPS)- induced acute kidney injury (AKI) in mice and explore its mechanism. METHODS: Forty male BALB/c mice were randomly divided into control group (with saline treatment), 15 mg/kg LPS group, and quercetin-treated groups with intragastric quercetin treatment (once daily for 3 consecutive days) at low (25 mg/kg) and high (50 mg/kg) dose prior to 15 mg/kg LPS injection. LPS was administered by intraperitoneally injection 1 after the last gavage of quercetin. The mice were sacrificed 24 h after LPS injection for analysis of kidney pathologies, blood urea nitrogen (BUN) and creatinine levels; serum levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and IL-6 were detected by ELISA, and the expressions of Toll-like receptor-4 (TLR4), MyD88, TRAF-6 and NF-κBp65 in the kidney were detected by Western blotting. RESULTS: Quercetin significantly lessened renal pathologies, lowered BUN and creatinine levels (P < 0.05) and inhibited TNF-α, IL-1ß, and IL-6 production in mice with LPS-induced AKI (P < 0.05). Pretreatment with quercetin also significantly inhibited TLR4, MyD88, and TRAF-6 expressions and NF-κBp65 activation in the kidneys of the rats with LPS challenge (P < 0.05). CONCLUSIONS: Quercetin pretreatment can protect mice against LPSinduced AKI by inhibiting TLR4/NF-κB signaling pathway.


Assuntos
Lesão Renal Aguda , Antioxidantes , Quercetina , Receptor 4 Toll-Like , Fator de Necrose Tumoral alfa , Animais , Antioxidantes/farmacologia , Lipopolissacarídeos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , NF-kappa B , Quercetina/farmacologia , Ratos , Receptor 4 Toll-Like/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos
14.
J Coll Physicians Surg Pak ; 29(6): 528-531, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31133150

RESUMO

OBJECTIVE: To investigate the effects of parecoxib on pain threshold and inflammatory factors interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in spinal cord of rats with bone cancer pain. STUDY DESIGN: An experimental study. PLACE AND DURATION OF STUDY: Department of Oncology, Shengjing Hospital of China Medical University, China, from March 2017 to May 2018. METHODOLOGY: Twenty-four healthy female Sprague-Dawley rats were selected and the bone cancer pain model was inoculated with W256 breast cancer cell into the bone marrow. Rats with bone cancer pain were randomly divided into the model group and the parecoxib group on the 7th day postoperation, with 12 rats in each group. Another 12 rats were taken as the control group. Rats in the parecoxib group were given intraperitoneal injection of parecoxib (8 mg/kg) for 10 consecutive days since the 15th day after operation. Mechanical pain threshold, thermal pain threshold, and the levels of inflammatory factors IL-1ß, IL-6 and TNF-α in spinal cord of rats in each group were compared. RESULTS: On the 14th postoperative day, mechanical pain threshold and thermal pain threshold of rats in the model group and the parecoxib group were significantly decreased compared with those in the control group (p<0.001). After 5 and 10 days of administration, mechanical and thermal pain threshold of rats in the parecoxib group were significantly higher than those in the model group and the control group (p<0.001). After 10 days of administration, levels of IL-1ß, IL-6 and TNF-α in spinal cord of the model group were higher than those of the control group (p<0.001); and levels of IL-1ß, IL-6 and TNF-α in spinal cord of the parecoxib group were significantly lower than those in the model group and the control group (p<0.001). CONCLUSION: Parecoxib can alleviate hyperalgesia in rats with bone cancer pain, increase pain threshold and inhibit the up-regulation of inflammatory factors in the spinal cord. Parecoxib may achieve analgesic effects by down-regulating the expression of IL-1ß, IL-6 and TNF-α in the spinal cord.


Assuntos
Dor do Câncer/tratamento farmacológico , Inibidores de Ciclo-Oxigenase 2/farmacologia , Interleucina-1beta/efeitos dos fármacos , Interleucina-6/líquido cefalorraquidiano , Isoxazóis/farmacologia , Limiar da Dor/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Animais , Neoplasias Ósseas/patologia , Inibidores de Ciclo-Oxigenase 2/administração & dosagem , Regulação para Baixo , Feminino , Hiperalgesia , Inflamação , Interleucina-1beta/líquido cefalorraquidiano , Isoxazóis/administração & dosagem , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Medula Espinal , Fator de Necrose Tumoral alfa/líquido cefalorraquidiano
15.
An Acad Bras Cienc ; 91(2): e20180699, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31038541

RESUMO

Besides stimulating vasoconstriction, Angiotensin II is also well known in inducing reactive oxygen species and promoting inflammatory phenotype switch via its type 1 receptor. In clinic, Angiotensin II type 1 (AT1) receptor blocker like candesartan has been widely applied as an antihypertensive medication. We previous have demonstrated that a higher dose of candesartan plays a protective role after kidney injury. However, whether candesartan could exhibit anti-inflammatory effects remains unclear. Here, by stimulating isolated human embryonic kidney epithelial cells with tumor necrosis factor-α (TNF-α), we observed the anti-inflammation capacity of candesartan ex vivo. It was found that pre-treat with candesartan significantly suppressed transforming growth factor-ß (TGF-ß) and interleukin-6 (IL-6) expression after incubation with TNF-α. Surprisingly, silence of angiotensin II type 1 receptor has little effects on reducing TGF-ß or IL-6 products. Furthermore, candesartan inhibited TNF-α-induced oxidative stress in the primary cultured tubular epithelial cells. Overall, our data indicates that candesartan suppresses TNF-α-induced inflammatory cytokine production by inhibiting oxidative stress, rather than block AT1 receptor activity.


Assuntos
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Benzimidazóis/farmacologia , Células Epiteliais/efeitos dos fármacos , Rim/citologia , Tetrazóis/farmacologia , Análise de Variância , Western Blotting , Células Cultivadas , Ensaio de Imunoadsorção Enzimática , Humanos , Interleucina-6/análise , Rim/embriologia , Linfotoxina-alfa/análise , Linfotoxina-alfa/efeitos dos fármacos , Espécies Reativas de Oxigênio/análise , Receptor Tipo 1 de Angiotensina/análise , Receptor Tipo 1 de Angiotensina/efeitos dos fármacos , Fator de Necrose Tumoral alfa/análise , Fator de Necrose Tumoral alfa/efeitos dos fármacos
16.
Life Sci ; 226: 149-155, 2019 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-30981764

RESUMO

AIMS: To investigate the effects and mechanisms of DLL3 in inflammation-mediated A2058 melanoma cell invasion and metastasis. MATERIALS AND METHODS: Melanoma A2058 cells was stimulated with lipopolysaccharide (LPS), with or without transfection of DLL3 siRNA, or DLL3 overexpression vector, or Twist1 siRNA. Cell migration and invasion were detected by wound healing and transwell invasion assay. The production of inflammatory factors TNF-α and IL-6 was measured by ELISA. The expression of Notch signaling-related molecules was detected by PCR and western blot. The protein expression of MMP1, MMP9, VEGF, DLL3, and EMT-related molecules was tested by western blot. KEY FINDINGS: LPS treatment increased migration and invasion of A2058 cells, accompanied by increased expression of TNF-α and IL-6. DLL3 was both upregulated in the LPS- or TNF-α-stimulated A2058 cells, and DLL3 knockdown inhibited LPS-induced inflammation, migration and invasion of A2058 cells, accompanied by down-regulation of MMP1, MMP9 and VEGF. Besides, DLL3 knockdown inhibits the expression of Twist1, a key EMT regulating factor, as well as the EMT hallmarks slug, N-cadherin and vimentin. Moreover, Twist1 silence inhibited EMT, and limited LPS-induced migration and invasion of A2058 cells, with decreased expression of MMP1, MMP9 and VEGF and reduced production of TNF-α and IL-6 in LPS-stimulated A2058 cells. SIGNIFICANCE: Knockdown of DLL3 restricts LPS-induced inflammation, migration and invasion of A2058 melanoma cells via blocking Twist1-mediated EMT. Therefore, targeting DLL3 may be a promising therapeutic strategy against inflammation-aggravated melanoma progression.


Assuntos
Peptídeos e Proteínas de Sinalização Intracelular/genética , Peptídeos e Proteínas de Sinalização Intracelular/fisiologia , Melanoma/metabolismo , Proteínas de Membrana/genética , Proteínas de Membrana/fisiologia , Caderinas , Linhagem Celular Tumoral , Movimento Celular/genética , Regulação para Baixo , Transição Epitelial-Mesenquimal/genética , Regulação Neoplásica da Expressão Gênica/genética , Técnicas de Silenciamento de Genes , Humanos , Inflamação/genética , Interleucina-6 , Lipopolissacarídeos/farmacologia , Metaloproteinase 1 da Matriz , Metaloproteinase 9 da Matriz , Melanoma/genética , Invasividade Neoplásica/genética , Proteínas Nucleares/fisiologia , Transdução de Sinais , Ativação Transcricional , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Proteína 1 Relacionada a Twist/fisiologia , Regulação para Cima , Fator A de Crescimento do Endotélio Vascular , Vimentina
17.
Mol Biol Rep ; 46(4): 3701-3711, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31006095

RESUMO

Nowadays, medicinal plants have been widely used everywhere to provide essential care for many disorders including diabetes. Recent reports assumed that the antidiabetic activities of pomegranate aril juice (PAJ) may be ascribed to its punicalagin (PCG). Therefore, the present study evaluated and compared the antidiabetic activities of PAJ and its PCG, and monitored some mechanisms of their actions in streptozotocin-nicotinamide (STZ-NA) type 2 diabetic rats. STZ-NA diabetic rats were given, orally/daily, PAJ (100 or 300 mg/kg body weight, containing 2.6 and 7.8 mg of PCG/kg body weight, respectively), pure PCG (2.6 or 7.8 mg/kg body weight), or distilled water (vehicle) for 6 weeks. PAJ (especially at the high dose) alleviated significantly (P < 0.05-0.001) most signs of type 2 diabetes including body-weight loss, insulin resistance (IR) and hyperglycemia through decreasing serum tumor necrosis factor-α concentration and the expression of hepatic c-Jun N-terminal kinase, and increasing the skeletal muscle weight and the expression of hepatic insulin receptor substrate-1 in STZ-NA diabetic rats. Also, it decreased significantly (P < 0.001) the oxidative liver injury in STZ-NA diabetic rats through decreasing the hepatic lipid peroxidation and nitric oxide production, and improving the hepatic antioxidant defense system. Although the low dose of PCG induced some modulation in STZ-NA diabetic rats, the high dose of PCG did not show any valuable antidiabetic activity, but induced many side effects. In conclusion, PAJ was safer and more effective than pure PCG in alleviating IR and oxidative liver injury in STZ-NA diabetic rats.


Assuntos
Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/metabolismo , Taninos Hidrolisáveis/administração & dosagem , Taninos Hidrolisáveis/uso terapêutico , Resistência à Insulina , Fígado/efeitos dos fármacos , Fígado/patologia , Niacinamida/administração & dosagem , Romã (Fruta)/metabolismo , Estreptozocina/administração & dosagem , Animais , Antioxidantes/metabolismo , Glicemia/metabolismo , Peso Corporal/efeitos dos fármacos , Taninos Hidrolisáveis/metabolismo , Hiperglicemia/tratamento farmacológico , Proteínas Substratos do Receptor de Insulina/efeitos dos fármacos , Proteínas Quinases JNK Ativadas por Mitógeno/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Masculino , Músculo Esquelético/efeitos dos fármacos , Niacinamida/metabolismo , Óxido Nítrico/metabolismo , Ratos , Estreptozocina/metabolismo , Fator de Necrose Tumoral alfa/efeitos dos fármacos
18.
J Coll Physicians Surg Pak ; 29(4): 345-348, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30925958

RESUMO

OBJECTIVE: To determine the effects of combined treatment of montelukast and budesonide on young children with cough variant asthma, and their serum inflammatory factors of serum hypersensitive c-reactive protein (hs-CRP), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and pulmonary function. STUDY DESIGN: An experimental study. PLACE AND DURATION OF STUDY: The Second Affiliated Hospital of Xi'an Jiaotong University, China, from January 2016 to January 2017. METHODOLOGY: A total of 112 children with cough variant asthma were randomly divided into observation group and control group with 56 cases in each group. All children were treated with antibiotics and resolving phlegm. The control group were given budesonide, while the observation group was treated additionally with montelukast. After the course, improvement time of clinical symptoms of cough, asthma, etc., changes in levels of serum inflammatory factors of hs-CRP, TNF-α and IL-6, and pulmonary function indexes of forced vital capacity (FVC), forced expiratory volume at the end of the first 1s (FEV1), peak expiratory flow (PEF), and observe concurrence of untoward effects in the two groups of sick children were compared. RESULTS: After treatment, extinction time for cough and for asthma of the observation group was less than those in the control group (all p<0.001). Levels of serum hs-CRP, TNF-α, IL-6 in the observation group were all lower than those of the control group (all p<0.001). Pulmonary function indices of FVC, FEV1 and PEF of the two groups of sick children were all higher than those of the control group (all p<0.001). During the treatment, there was no difference in the comparison of untoward effect rate of the two groups (p=0.696). After follow-up observation on the two groups of sick children for 1 year, the recurrence rate of the observation group was lower than that of the control group (p=0.026). CONCLUSION: Curative effects on young children with cough variant asthma of montelukast combined with budesonide are significant. The therapy may improve clinical symptoms and pulmonary function and reduce serum inflammatory factor level of sick children, with high application value and worthy of application and promotion.


Assuntos
Acetatos/administração & dosagem , Antiasmáticos/administração & dosagem , Anti-Inflamatórios/administração & dosagem , Asma/tratamento farmacológico , Budesonida/administração & dosagem , Tosse/tratamento farmacológico , Pulmão/fisiopatologia , Quinolinas/administração & dosagem , Antiasmáticos/efeitos adversos , Anti-Inflamatórios/efeitos adversos , Budesonida/efeitos adversos , Proteína C-Reativa/efeitos dos fármacos , Proteína C-Reativa/metabolismo , Criança , Pré-Escolar , Tosse/complicações , Feminino , Humanos , Interleucina-6/sangue , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Masculino , Testes de Função Respiratória , Resultado do Tratamento , Fator de Necrose Tumoral alfa/sangue , Fator de Necrose Tumoral alfa/efeitos dos fármacos
19.
J Eur Acad Dermatol Venereol ; 33(11): 2197-2201, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30835878

RESUMO

BACKGROUND: While increased levels of circulating inflammatory cytokines in chronologically aged humans have been linked to the development of ageing-associated chronic disorders (e.g., cardiovascular disease, type II diabetes, osteoporosis and Alzheimer's disease), approaches that reduce circulating cytokines are not yet available. In chronologically aged mice, we recently demonstrated that epidermal dysfunction largely accounts for age-associated elevations in circulating cytokine levels, and that improving epidermal function reduced circulating cytokine levels. OBJECTIVE: We performed a pilot study to determine whether improving epidermal function reduces circulating pro-inflammatory cytokine levels in aged humans. METHODS: Thirty-three aged humans were topically treated twice-daily for 30 days, with ≈ 3 mL of an emollient, previously shown to improve epidermal function, while untreated, aged humans and a cohort of young volunteers served as controls. Changes in epidermal function and levels of three key, age-related, plasma cytokines (IL-1ß, IL-6 and TNFα) were measured at baseline and after treatment, using Luminex 200™ system. RESULTS: We also found significantly higher baseline levels of IL-1ß, IL-6 and TNFα in aged vs. young humans (P < 0.001), as previously reported. Topical applications of the barrier repair emollient significantly enhanced epidermal permeability barrier function (P < 0.01) and stratum corneum hydration (P < 0.05). In parallel, circulating levels of IL-1ß and IL-6 normalized, while TNFα levels declined substantially. CONCLUSION: The results of this preliminary study suggest that a larger clinical trial should be performed to confirm whether improving epidermal function also can reduce circulating pro-inflammatory cytokine levels in aged humans, while also possibly attenuating the downstream development of chronic inflammatory disorders in the aged humans.


Assuntos
Emolientes/administração & dosagem , Interleucina-1beta/sangue , Interleucina-1beta/efeitos dos fármacos , Interleucina-6/sangue , Fenômenos Fisiológicos da Pele/efeitos dos fármacos , Fator de Necrose Tumoral alfa/sangue , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Administração Tópica , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Emolientes/farmacologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Projetos Piloto
20.
Artigo em Chinês | MEDLINE | ID: mdl-30813699

RESUMO

Objective:To observe the effect of 18ß-sodium glycyrrhetinic acid(18ß-SGA) on the expression of TNF-α in nasal mucosa of rats with allergic rhinitis(AR), and explore the intervention mechanism of 18ß-SGA on AR. Method:One hundred and six SPF-level Wistar rats were randomly divided into control group, AR group, budesonide group, 18ß-SGA low dose group and high dose group. After the AR rat model was constructed by ovalbumin, the rats were given drug intervention and sacrificed after 2 and 4 weeks of intervention. The nasal mucosa of the rats was taken for immunohistochemical staining, RT-qPCR and Western-blotting to localize and quantify the expression of TNF-α. Result:By immunohistochemistry, Western-blotting and RT-PCR, TNF-α was mainly found in the columnar epithelium, vascular endothelium, glandular and some inflammatory cytoplasm of nasal mucosa. And the expression of TNF-α in the nasal mucosa of AR rats was significantly increased than the normal group at the protein and mRNA levels (P<0.01). After intervention with different doses of 18ß-SGA, the expression of TNF-α was significantly decreased (P<0.01), especially after 4 weeks of 18ß-SGA low dose group(P<0.01). Conclusion:Different doses of 18ß-SGA have therapeutic effects on AR, and its mechanism of action may be related to the inhibition of TNF-α expression.


Assuntos
Anti-Inflamatórios , Ácido Glicirretínico , Rinite Alérgica , Fator de Necrose Tumoral alfa , Animais , Anti-Inflamatórios/farmacologia , Modelos Animais de Doenças , Ácido Glicirretínico/farmacologia , Mucosa Nasal , Distribuição Aleatória , Ratos , Ratos Wistar , Rinite Alérgica/tratamento farmacológico , Rinite Alérgica/metabolismo , Sódio , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo
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