Exendin-4 attenuates lipopolysaccharides induced inflammatory response but does not protects H9c2 cells from apoptosis

Tien Hsing Chen, Hung Ta Wo, Chien Chia Wu, Jian Liang Wang, Chun Chieh Wang, I. Chang Hsieh, Cheng Yi Kuo, Chien Ting Liu*

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

10 引文 斯高帕斯(Scopus)

摘要

Background: Glucagon-like peptide-1 (GLP-1) and its analogues are reported to exert wide-ranging cardiovascular actions in preclinical and clinical studies. We thus investigated whether the GLP-1 receptor agonist, exendin-4, has inhibitory effects on LPS-stimulated inflammatory response in cardiomyoblasts. Methods: H9c2 cardiomyoblasts were exposed to LPS and treated with exendin-4. Expressions of proinflammatory mediators were assessed using quantitative real-time PCR. Nuclear localization of NF-κB was examined using immunoblotting. mRNA expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production were evaluated by q PCR and NO assay. Furthermore, anti-apoptotic effect of exendin-4 in LPS-stimulated H9c2 cells was determined using qPCR and immunoblot. Results: Exposure to LPS increased mRNA expressions of TNF-α, COX-2 and MMP-9 in H9c2 cells. It also caused increases in iNOS mRNA expression and NF-κB nuclear translocation. Exendin-4 dose-dependently downregulated mRNA levels of TNF-α, COX-2 and MMP-9 in LPS-stimulated H9c2 cells. It also reduced NF-κB nuclear translocation. Treatment with exendin-4 showed no effect on LPS-induced apoptosis in H9c2 cells. Conclusions: Exendin-4 exerts an effect on cardiomyoblast exposed to LPS by inhibiting mRNA expression of inflammatory mediators and suppressing NF-κB activation. These effects are consistent with some of the observed anti-inflammatory properties of exendin-4, as well as its beneficial actions on the cardiovascular system.

原文英語
頁(從 - 到)484-490
頁數7
期刊Immunopharmacology and Immunotoxicology
34
發行號3
DOIs
出版狀態已出版 - 06 2012

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