Traditional Chinese Medication Qiliqiangxin Protects Against Cardiac Remodeling and Dysfunction in Spontaneously Hypertensive Rats

被引:32
|
作者
Wang, Hui [1 ,2 ]
Zhang, Xiaomin [1 ,2 ]
Yu, Pujiao [3 ]
Zhou, Qiulian [4 ,5 ]
Zhang, Jialiang [1 ,2 ]
Zhang, Haifeng [1 ]
Zhu, Hongsheng [6 ]
Zhang, Chenlin [6 ]
Yao, Wenming [1 ]
Che, Lin [3 ]
Xu, Jiahong [3 ]
Bei, Yihua [4 ,5 ]
Li, Xinli [1 ]
机构
[1] Nanjing Med Univ, Dept Cardiol, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Jiangsu Shengze Hosp, Dept Cardiol, Suzhou 215228, Peoples R China
[3] Tongji Univ, Tongji Hosp, Dept Cardiol, Sch Med, Shanghai 200065, Peoples R China
[4] Shanghai Univ, Sch Life Sci, Cardiac Regenerat & Ageing Lab, 333 Nan Chen Rd, Shanghai 200444, Peoples R China
[5] Shanghai Univ, Innovat Drug Res Ctr, Shanghai 200444, Peoples R China
[6] Shanghai Univ Tradit Chinese Med, Longhua Hosp, Dept Anesthesiol, Shanghai 200032, Peoples R China
来源
INTERNATIONAL JOURNAL OF MEDICAL SCIENCES | 2017年 / 14卷 / 05期
基金
中国国家自然科学基金;
关键词
Qiliqiangxin; cardiac remodeling; fibrosis; spontaneously hypertension; PPAR; PGC-1; alpha; DIASTOLIC HEART-FAILURE; FATTY-ACID OXIDATION; ALPHA PPAR-ALPHA; PRESSURE-OVERLOAD; MICE; FIBROSIS; GAMMA; CARDIOMYOCYTES; HYPERTROPHY; BETA/DELTA;
D O I
10.7150/ijms.18142
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Qiliqiangxin (QLQX), a traditional Chinese herbs medication, exerted protective effect in chronic heart failure patients in a multicenter randomized double-blind study. QLQX has also been found to improve cardiac function and reduce cardiac fibrosis in spontaneously hypertension animal model. However, the effect of longterm treatment with QLQX in such a condition and the related molecular mechanisms remain largely unknown. In the present study, thirteen-week-old spontaneously hypertensive rats (SHRs) were treated by daily intragastric administration of QLQX or saline for one year. Echocardiography, electron microscopy, and Masson's trichrome staining were used to determine cardiac function, mitochondria ultrastructure, and cardiac fibrosis, respectively. Quantitative reverse transcription polymerase chain reactions (qRT-PCRs) and Western blotting were used to determine gene expressions. We found that QLQX significantly improved cardiac function and reduced gene markers of pathological hypertrophy including ANP, BNP, and Myh7. QLQX also attenuated cardiac fibrosis and apoptosis in SHRs as evidenced by downregulation of alpha-SMA, collagen I, collagen III, and TGF-beta expressions and reduction of Bax to Bcl-2 ratio. Moreover, the damage of mitochondrial ultrastructure was greatly improved and the reduction of PPAR-alpha, PPAR-gamma, and PGC-1 alpha expression levels was significantly restored in SHRs by treatment with QLQX. In conclusion, longterm treatment with QLQX protects against cardiac remodeling and dysfunction in hypertension by increasing PPARs and PGC-1 alpha.
引用
收藏
页码:506 / 514
页数:9
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