MEF2C公司
苯肾上腺素
体内
HDAC4型
免疫荧光
心肌细胞
污渍
肌肉肥大
信号转导
细胞生物学
体外
药理学
化学
医学
分子生物学
生物
基因表达
生物化学
内科学
基因
免疫学
抗体
生物技术
组蛋白甲基转移酶
血压
作者
Xueqin Li,Shuang Liu,L. Xia,Xiaoli Shan,Wenxia Zhao,Huihua Chen,Chen Zhang,Wei Guo,Ming Xu,Rong Lü,Pei Zhao
出处
期刊:PubMed
日期:2022-01-01
卷期号:14 (6): 3840-3853
摘要
Stachydrine hydrochloride (Sta), an activated alkaloid, is isolated from traditional Chinese medicine Yimucao. In previous studies, the cardioprotective effects of Sta were found in our laboratory. However, the underling mechanisms of Sta is not fully elucidated. The aim of this study was to provide a detailed account of the anti-hypertrophic effects of Sta on transcriptional regulation. In vivo, C57BL/6J mice were subjected to transverse aortic constriction (TAC) and were orally treated with Sta. Morphological assessments, echocardiographic parameters, histological analyses and immunofluorescence were used to evaluate cardiac hypertrophy. In vitro, cardiomyocytes were stimulated by phenylephrine (PE), and cell surface and hypertrophy markers were tested by immunofluorescence and real-time polymerase chain reaction (RT-PCR). Moreover, western blotting, RT-PCR and luciferase reporter genes were used to assess the expression of proteins, mRNA and the activity of the CaMKII/HDAC4/MEF2C signal pathway in vivo and in vitro. We found that Sta blocked cardiac hypertrophy induced by pressure overload. We also demonstrated that Sta inhibited nuclear export or promoted nuclear import of HDAC4 through regulation of p-CaMKII, and it further improved the repression of MEF2C. Taken together, our findings demonstrated that Sta ameliorates cardiac hypertrophy through CaMKII/HDAC4/MEF2C signal pathway.
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