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Abstract Title:

Favorable effects of resveratrol on sympathetic neural remodeling in rats following myocardial infarction.

Abstract Source:

Eur J Pharmacol. 2010 Dec 15;649(1-3):293-300. Epub 2010 Sep 24. PMID: 20869962

Abstract Author(s):

Ping Xin, Yesheng Pan, Wei Zhu, Shian Huang, Meng Wei, Can Chen

Article Affiliation:

Division of Cardiology, Shanghai Sixth Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

Abstract:

Oxidative stress and inflammatory response induced by myocardial infarction play important roles in the development of sympathetic neural remodeling. The present study was designed to investigate whether resveratrol can improve sympathetic neural remodeling and hence cause less arrhythmias via its anti-oxidant and anti-inflammatory effects. Male Sprague Dawley rats were randomly assigned to either vehicle or resveratrol (1 mg/kg) treatment for 4 weeks post myocardial infarction. Another group of sham operated rats served as controls. Cardiac electrophysiology examination was performed to evaluate the severity of ventricular arrhythmias. Sympathetic neural remodeling characterized by heterogeneous nerve sprouting and sympathetic hyperinnervation was assessed by immunohistochemistry study. Western blotting and ELISA were used to evaluate inflammatory responses and oxidative stress was also quantified. Resveratrol treatment resulted in less episodes of inducible ventricular arrhythmias which was closely associated with attenuated sympathetic neural remodeling (P<0.001, respectively). Decreased nerve growth factor (NGF) expression was also observed in resveratrol treated rats in the peri-infarct area at 4 weeks after myocardial infarction (P<0.001). Interestingly, beneficial effects of resveratrol were also associated with less inflammatory responses and oxidative stress. Our data indicated that resveratrol can suppress sympathetic neural remodeling process after myocardial infarction via attenuated inflammatory responses and oxidative stress, which in turn leads to less inducibility of ventricular arrhythmias.

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