Shensongyangxin protects against pressure overload-induced cardiac hypertrophy

被引:12
|
作者
Shen, Di-Fei [1 ,2 ,3 ]
Wu, Qing-Qing [1 ,3 ]
Ni, Jian [1 ,3 ]
Deng, Wei [1 ,3 ]
Wei, Cong [4 ]
Jia, Zhen-Hua [4 ]
Zhou, Heng [1 ,3 ]
Zhou, Meng-Qiao [1 ,3 ]
Bian, Zhou-Yan [1 ,3 ]
Tang, Qi-Zhu [1 ,3 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Cardiol, Wuhan 430060, Hubei, Peoples R China
[2] Xinjiang Med Univ, Teaching Hosp 5, Dept Cardiol, Xinjiang 830011, Chinese Autonom, Peoples R China
[3] Wuhan Univ, Cardiovasc Res Inst, Wuhan 430060, Hubei, Peoples R China
[4] Integrat Tradit & Western Med Res Acad Hebei, Shijiazhuang 050035, Hebei, Peoples R China
关键词
shensongyangxin; cardiac hypertrophy; cardiac fibrosis; Akt; transforming growth factor beta/small mothers against decapentaplegic;
D O I
10.3892/mmr.2015.4598
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Shensongyangxin (SSYX) is a medicinal herb, which has long been used in traditional Chinese medicine. Various pharmacological activities of SSYX have been identified. However, the role of SSYX in cardiac hypertrophy remains to be fully elucidated. In present study, aortic banding (AB) was performed to induce cardiac hypertrophy in mice. SSYX (520 mg/kg) was administered by daily gavage between 1 and 8 weeks following surgery. The extent of cardiac hypertrophy was then evaluated by pathological and molecular analyses of heart tissue samples. In addition, in vitro experiments were performed to confirm the in vivo results. The data of the present study demonstrated that SSYX prevented the cardiac hypertrophy and fibrosis induced by AB, as assessed by measurements of heart weight and gross heart size, hematoxylin and eosin staining, cross-sectional cardiomyocyte area and the mRNA expression levels of hypertrophic markers. SSYX also inhibited collagen deposition and suppressed the expression of transforming growth factor beta (TGF beta), connective tissue growth factor, fibronectin, collagen I alpha and collagen III alpha, which was mediated by the inhibition of the TGF beta/small mothers against decapentaplegic (Smad) signaling pathway. The inhibitory action of SSYX on cardiac hypertrophy was mediated by the inhibition of Akt signaling. In vitro investigations in the rat H9c2 cardiac cells also demonstrated that SSYX attenuated angiotensin II-induced cardiomyocyte hypertrophy. These findings suggested that SSYX attenuated cardiac hypertrophy and fibrosis in the pressure overloaded mouse heart. Therefore, the cardioprotective effect of SSYX is associated with inhibition of the Akt and TGF beta/Smad signaling pathways.
引用
收藏
页码:980 / 988
页数:9
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