Traditional Chinese medicine Qiliqiangxin attenuates phenylephrine-induced cardiac hypertrophy via upregulating PPARγ and PGC-1α

被引:23
作者
Gao, Rong-Rong [1 ]
Wu, Xiao-Dong [1 ]
Jiang, Hui-Min [2 ]
Zhu, Yu-Jiao [3 ]
Zhou, Yan-Li [1 ]
Zhang, Hai-Feng [1 ]
Yao, Wen-Ming [1 ]
Li, Yong-Qin [3 ]
Li, Xin-Li [1 ]
机构
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Cardiol, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China
[2] Beijing Hosp Tradit Chinese Med, Clin Lab Ctr, Beijing 100010, Peoples R China
[3] Shanghai Univ, Expt Ctr Life Sci, Inst Cardiovasc Sci, Cardiac Regenerat & Ageing Lab,Sch Life Sci, Shanghai 200444, Peoples R China
基金
中国国家自然科学基金;
关键词
Cardiac hypertrophy; PPAR gamma; PGC-1; alpha; Qiliqiangxin (QLQX); ACTIVATED RECEPTOR-GAMMA; ISCHEMIA-REPERFUSION INJURY; HEART-FAILURE; MEDICATION QILIQIANGXIN; MYOCARDIAL-INFARCTION; ENERGY-METABOLISM; IN-VIVO; MICE; DYSFUNCTION; PHOSPHORYLATION;
D O I
10.21037/atm.2018.04.14
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: Clinical study has demonstrated that the traditional Chinese medicine Qiliqiangxin (QLQX) has protective effects on heart failure. Phenylephrine (PE) is an important inducing factor for cardiac hypertrophy and our previous studies have showed that QLQX attenuates PE-induced cardiac hypertrophy. Besides, QLQX protects against cardiac remodeling after myocardial infarction via activating PPAR gamma. However, whether QLQX prevents PE-induced cardiac hypertrophy through PPAR gamma and its coactivator PGC-1 alpha is still unknown. Methods: The effects of QLQX were investigated based on PE-induced cardiac hypertrophy mouse models. Echocardiography and hematoxylin-eosin (HE) staining were used to determine cardiac function and cross-sectional area, respectively. Quantitative real time PCR (qRT-PCR) was used to determine ANP and BNP expressions. Based on primary neonatal rat ventricular cardiomyocytes (NRVMs) treated with PE, the cell size and expressions of ANP and BNP were determined by immunofluorescent staining and qRT-PCR, respectively. In addition, western blot was used to determine PPAR gamma and PGC-1 alpha expressions. Results: In present study, we confirmed that QLQX could significantly attenuate cardiac hypertrophy in mice treated with PE. Then we showed that PPAR gamma and PGC-1 alpha were downregulated in PE-induced cardiac hypertrophy, and QLQX could block the decrease of PPAR gamma and PGC-1 alpha both in vitro and in vivo. Importantly, we found that PPAR gamma inhibitors or PGC-1 alpha siRNAs eliminated the protective effects of QLQX on PE-induced cardiac hypertrophy. Conclusions: Our study suggested that QLQX prevents from PE-induced cardiac hypertrophy by activating PPAR gamma and its coactivator PGC-1 alpha.
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页数:9
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