Int J Med Sci 2017; 14(5):506-514. doi:10.7150/ijms.18142 This issue
1. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China;
2. Department of Cardiology, Jiangsu Shengze Hospital, Nanjing Medical University, Suzhou 215228, China;
3. Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China;
4. Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai 200444, China;
5. Innovative Drug Research Center of Shanghai University, Shanghai 200444, China;
6. Department of Anesthesiology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
* These three authors contributed equally to this work.
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 α-SMA, collagen I, collagen III, and TGF-β expressions and reduction of Bax to Bcl-2 ratio. Moreover, the damage of mitochondrial ultrastructure was greatly improved and the reduction of PPAR-α, PPAR-γ, and PGC-1α 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-1α.
Keywords: Qiliqiangxin, cardiac remodeling, fibrosis, spontaneously hypertension, PPAR, PGC-1α.