Shenfu Injection attenuates rat myocardial hypertrophy by up-regulating miR-19a-3p expression

被引:23
|
作者
Mao, Zhu-Jun [1 ]
Zhang, Quan-Long [1 ]
Shang, Jia [2 ]
Gao, Ting [2 ]
Yuan, Wen-Jun [2 ,3 ]
Qin, Lu-Ping [1 ]
机构
[1] Zhejiang Chinese Med Univ, Sch Pharm, Dept Pharmacognosy, Hangzhou 310053, ZJ, Peoples R China
[2] Ningxia Med Univ, Dept Physiol, Yinchuan 750004, NX, Peoples R China
[3] Second Mil Med Univ, Dept Physiol, Shanghai 200433, Peoples R China
来源
SCIENTIFIC REPORTS | 2018年 / 8卷
基金
中国国家自然科学基金;
关键词
CARDIAC-HYPERTROPHY; GENE; MICRORNAS; CHANNELS; HEART; TRPC1; MEF2A;
D O I
10.1038/s41598-018-23137-4
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Shenfu Injection (SFI) is a classical Chinese medicine used to treat heart failure. Our previous study demonstrated that miRNAs underwent changes in rats with myocardial hypertrophy induced by abdominal aortic constriction. Interestingly, there was a significant change in miR-19a-3p, whose target gene is known to be associated with MEF2 signaling. However, whether and how SFI regulates miR-19a-3p in the treatment of myocardial hypertrophy has not been investigated. The purpose of the present study was to investigate the regulatory effect of SFI on miR-19a-3p in MEF2 signaling in the rat hypertrophic myocardium. We found that the miR-19a-3p expression level was significantly decreased in the hypertrophic myocardium, and MEF2A was the target gene of miR-19a-3p. The protein expressions of MEF2A, beta-MHC, BNP and TRPC1 were significantly increased in hypertrophic cardiomyocytes. MiR-19a-3p was up-regulated after SFI treatment, and the protein expressions of these genes were significantly decreased. In addition, miR-19a-3p over-expression in hypertrophic cardiomyocytes could decrease MEF2A mRNA and protein expressions, and anti-miR-19a-3p showed the opposite result. Our study provided substantial evidence that miR-19a-3p played a functional role in MEF2 signaling in myocardial hypertrophy. SFI attenuated cardiomyocyte hypertrophy probably through up-regulating or maintaining the miR-19a-3p levels and regulating the MEF2 signaling pathway.
引用
收藏
页数:11
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