Atorvastatin attenuates myocardial remodeling induced by chronic intermittent hypoxia in rats: Partly involvement of TLR-4/MYD88 pathway

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• 作者：Xiao Yuan¹ ; Yan Deng¹ ; Xueling Guo ; Jin Shang ; Die Zhu ; Huiguo Liu ; ^{hgliu@tjh.tjmu.edu.cn" class="auth_mail}
• 关键词：Atorvastatin ; Chronic intermittent hypoxia ; Inflammatory response ; Cardiac hypertrophy ; Toll-like receptor 4
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：28 March, 2014
• 年：2014
• 卷：446
• 期：1
• 页码：292-297
• 全文大小：1432 K

文摘

Inflammatory processes and oxidative stress are known to play a key role in the development of cardiovascular complications such as cardiac hypertrophy induced by chronic intermittent hypoxia (CIH), the most characteristic pathophysiological change of obstructive sleep apnea syndrome (OSAS). Current evidence suggests that competitive inhibitors of 3-hydroxy-3-methylglutaryl-CoA coenzyme A reductase, such as atorvastatin, not only reduce blood lipids but also have anti-inflammatory and inhibit oxidative stress benefits. This study examined the protective role of atorvastatin in CIH-induced cardiac hypertrophy. Adult male wistar rats were subjected to 8 h of intermittent hypoxia/day, with/without atorvastatin for 6 weeks. Ventricular remodeling, toll-like receptor 4 (TLR-4), myeloid differentiation primary response protein 88 (MYD88), inflammatory agents and radical oxygen species were determined. As a result, we found that treatment with atorvastatin markedly inhibited the mRNA and protein expressions of TLR4, MYD88 and the downstream inflammatory agents and radical oxygen species. Administration of atorvastatin following CIH significantly ameliorated the myocardial injury, such as cardiac hypertrophy. In conclusion, Pre-CIH atorvastatin administration may attenuate TLR-4/MYD88 mediated inflammatory processes and oxidative stress in the injured rat myocardium, and this may be one mechanism by which atorvastatin ameliorated myocardial injury following CIH.