Curcumin protects against myocardial infarction-induced cardiac fibrosis via SIRT1 activation in vivo and in vitro

被引:115
|
作者
Xiao, Jie
Sheng, Xi
Zhang, Xinyu
Guo, Mengqi
Ji, Xiaoping [1 ,2 ]
机构
[1] Shandong Univ, Qilu Hosp, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Minist Educ, 107 Wenhua Xilu, Jinan 250012, Shandong, Peoples R China
[2] Shandong Univ, Qilu Hosp, Chinese Minist Hlth, 107 Wenhua Xilu, Jinan 250012, Shandong, Peoples R China
来源
DRUG DESIGN DEVELOPMENT AND THERAPY | 2016年 / 10卷
基金
中国国家自然科学基金;
关键词
curcumin; myocardial infarction; angiotensin II; cardiac fibroblasts; fibrosis; SIRT1; NF-KAPPA-B; DYSFUNCTION; RATS; REPERFUSION; INHIBITION; ISCHEMIA; PATHWAY; DISEASE; STRESS; INJURY;
D O I
10.2147/DDDT.S104925
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Curcumin, a polyphenolic compound derived from turmeric, protects against myocardial injury by alleviating oxidative stress, inflammation, apoptosis, and fibrosis. However, the role of curcumin and its mechanism of action on interstitial fibrosis after myocardial infarction (MI) are poorly understood. To clarify, MI was induced by a permanent ligation of the left anterior descending coronary artery in adult mice, and the effects of curcumin were evaluated 4 weeks after the MI event. In vitro, we treated cardiac fibroblasts (CFs) with Ang II, and investigated the anti-fibrotic mechanism of curcumin. Our results showed that curcumin significantly attenuated collagen deposition in vivo and inhibited CF proliferation and migration, and MMP expression. In addition, we found that the down-regulation of SIRT1 after MI was attenuated by curcumin pretreatment, which indicated that the activation of SIRT1 might be involved in the protective action of curcumin. This hypothesis was confirmed by genetic inhibition of SIRT1 (siRNA-SIRT1) in Ang II-treated CFs. Our results provide new insights into the mechanism underlying the anti-fibrotic effects of curcumin in the heart.
引用
收藏
页码:1267 / 1277
页数:11
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