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Acta Biochim Biophys Sin (Shanghai) ; 51(4): 347-355, 2019 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-30877771

RESUMO

Long-time consumption of high-fat food is a direct cause of cardiovascular diseases, and high-fat-related inflammation plays an important role in it. Toll-like receptors (TLRs), especially TLR2 and TLR4, play important roles in high-fat-related inflammation. However, the impact of TLR2 on high-fat-associated cardiovascular complications is still unknown. In this study, we try to investigate the relationship between TLR2 and high-fat-related cardiac injury. SD rats were allocated to either a control group which were fed with normal diet or a high-fat group which were fed with high-fat diet for 5 months. At the last month, rats fed with high-fat diet were intraperitoneally injected with control normal mouse IgG or anti-TLR2 antibody. Heart tissues were collected for further analysis. RT-qPCR and western blot analysis results revealed that TLR2 expression was increased in the heart tissues from rats fed with high-fat diet and anti-TLR2 antibody had no effect on TLR2 expression. However, anti-TLR2 antibody alleviated masson staining area, levels of TGF-ß1 and Collagen I mRNA, and decreased TUNEL-positive myocardial cells and caspase-3 activity, suggesting that anti-TLR2 antibody protected cardiac cells against high-fat-induced cardiac fibrosis and cell apoptosis. By using immunohistochemistry, RT-qPCR and ELISA, we found that anti-TLR2 antibody blocked NF-κB activation, inhibited the expression of inflammatory factors such as TNF-α, IL-1ß, IL-6 and IL-18 in the heart tissues from rats fed with high-fat diet. These results hinted that anti-TLR2 antibody might exert its protective effect via inhibition of the TLR2/NF-κB/inflammation pathway. Our findings suggest that anti-TLR2 antibody has a preventive function against high-fat-induced deleterious effects in the heart, and anti-TLR2 antibody may be used as an attractive therapeutic option for high-fat-induced cardiac injury.


Assuntos
Anticorpos/farmacologia , Cardiomiopatias/prevenção & controle , NF-kappa B/antagonistas & inibidores , Receptor 2 Toll-Like/genética , Animais , Anticorpos/imunologia , Apoptose/efeitos dos fármacos , Apoptose/genética , Cardiomiopatias/etiologia , Cardiomiopatias/metabolismo , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Citocinas/genética , Citocinas/metabolismo , Dieta Hiperlipídica/efeitos adversos , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Mediadores da Inflamação/metabolismo , Masculino , Camundongos Endogâmicos BALB C , NF-kappa B/genética , NF-kappa B/metabolismo , Ratos Sprague-Dawley , Receptor 2 Toll-Like/imunologia , Receptor 2 Toll-Like/metabolismo , Fator de Crescimento Transformador beta1/genética , Fator de Crescimento Transformador beta1/metabolismo
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