Gastrodin protects against cardiac hypertrophy and fibrosis

被引:83
作者
Shu, Chunming [1 ,2 ]
Chen, Changgui [1 ,2 ]
Zhang, Da-Ping [1 ,2 ]
Guo, Haipeng [1 ,2 ]
Zhou, Heng [1 ,2 ]
Zong, Jing [1 ,2 ]
Bian, Zhouyan [1 ,2 ]
Dong, Xuan [2 ]
Dai, Jia [1 ,2 ]
Zhang, Yan [1 ,2 ]
Tang, Qizhu [1 ,2 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Cardiol, Wuhan 430060, Peoples R China
[2] Wuhan Univ, Cardiovasc Res Inst, Wuhan 430060, Peoples R China
基金
中国国家自然科学基金;
关键词
Gastrodin; Cardiac hypertrophy; Fibrosis; ERK1/2; RAT; PHOSPHORYLATION; GATA4;
D O I
10.1007/s11010-011-0992-1
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Phenolic glucoside gastrodin (Gas), which is a main component extracted from the Chinese herbs Gastrodia elata Bl, is a well-known natural calcium antagonist with antioxidant and anti-inflammatory functions. It has long been used clinically for treatment of cardiovascular and cerebrovascular diseases. Previous studies have shown that gastrodin possesses comprehensive pharmacological functions. However, very little is known about whether gastrodin has protective role on cardiac hypertrophy. The aim of this study was to determine whether gastrodin attenuates pressure overload-induced cardiac hypertrophy in mice and to clarify the underlying molecular mechanisms. Our data demonstrated that gastrodin prevented cardiac hypertrophy induced by aortic banding (AB), as assessed by heart weight/body weight and lung weight/body weight ratios, echocardiographic parameters, and gene expression of hypertrophic markers. The inhibitory effect of gastrodin on cardiac hypertrophy is mediated by ERK1/2 signaling and GATA-4 activation. Further studies showed that gastrodin attenuated fibrosis and collagen synthesis through abrogating ERK1/2 signaling pathway. Therefore, these findings indicated that gastrodin, which is a potentially safe and inexpensive therapy for clinical use, has protective potential in targeting cardiac hypertrophy and fibrosis through suppression of ERK1/2 signaling.
引用
收藏
页码:9 / 16
页数:8
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