Gao Rong-Rong, Wu Xiao-Dong, Jiang Hui-Min, Zhu Yu-Jiao, Zhou Yan-Li, Zhang Hai-Feng, Yao Wen-Ming, Li Yong-Qin, Li Xin-Li
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Clinical Laboratory Center, Beijing Hospital of Traditional Chinese Medicine, Beijing 100010, China.
Ann Transl Med. 2018 Apr;6(8):153. doi: 10.21037/atm.2018.04.14.
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 PPARγ. However, whether QLQX prevents PE-induced cardiac hypertrophy through PPARγ and its coactivator PGC-1α is still unknown.
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 PPARγ and PGC-1α expressions.
In present study, we confirmed that QLQX could significantly attenuate cardiac hypertrophy in mice treated with PE. Then we showed that PPARγ and PGC-1α were downregulated in PE-induced cardiac hypertrophy, and QLQX could block the decrease of PPARγ and PGC-1α both and . Importantly, we found that PPARγ inhibitors or PGC-1α siRNAs eliminated the protective effects of QLQX on PE-induced cardiac hypertrophy.
Our study suggested that QLQX prevents from PE-induced cardiac hypertrophy by activating PPARγ and its coactivator PGC-1α.
临床研究表明，中药芪苈强心（QLQX）对心力衰竭具有保护作用。去甲肾上腺素（PE）是心脏肥大的重要诱导因素，我们之前的研究表明，QLQX可减轻PE诱导的心脏肥大。此外，QLQX通过激活PPARγ预防心肌梗死后的心脏重塑。然而，QLQX是否通过PPARγ及其共激活因子PGC-1α预防PE诱导的心脏肥大仍不清楚。
基于PE诱导的心脏肥大小鼠模型研究QLQX的作用。分别采用超声心动图和苏木精-伊红（HE）染色测定心脏功能和横截面积。采用定量实时PCR（qRT-PCR）测定ANP和BNP的表达。基于用PE处理的原代新生大鼠心室心肌细胞（NRVMs），分别通过免疫荧光染色和qRT-PCR测定细胞大小以及ANP和BNP的表达。此外，采用蛋白质印迹法测定PPARγ和PGC-1α的表达。
在本研究中，我们证实QLQX可显著减轻PE处理小鼠的心脏肥大。然后我们表明，在PE诱导的心脏肥大中PPARγ和PGC-1α下调，并且QLQX可阻止PPARγ和PGC-1α的降低。重要的是，我们发现PPARγ抑制剂或PGC-1α siRNA消除了QLQX对PE诱导的心脏肥大的保护作用。
我们的研究表明，QLQX通过激活PPARγ及其共激活因子PGC-1α预防PE诱导的心脏肥大。
