The protective effects of compatibility of Aconiti Lateralis Radix Praeparata and Zingiberis Rhizoma on rats with heart failure by enhancing mitochondrial biogenesis via Sirt1/PGC-1α pathway

线粒体生物发生 心力衰竭 医学 尼泊尔卢比1 乳酸脱氢酶 药理学 线粒体 心功能曲线 西妥因1 肌酸激酶 内科学 化学 生物化学 基因 下调和上调
作者
Xiaohua Lu,Lu Zhang,Pengyan Li,Jiabo Wang,Ruisheng Li,Yin-Qiu Huang,Mingquan Wu,Houqin Zhou,Yang Li,Shizhang Wei,Kun Li,Haotian Li,Xue-lin Zhou,Yan Zhao,Xiaohe Xiao
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier]
卷期号:92: 651-660 被引量:37
标识
DOI:10.1016/j.biopha.2017.05.117
摘要

Aconiti Lateralis Radix Praeparata (“Fuzi” in Chinese) in combination with Zingiberis Rhizoma (“Ganjiang” in Chinese) is commonly applied for the treatment of heart failure for thousands of years in China. However, its therapeutic mechanism is still poorly defined. This study aimed to investigate whether the compatibility of Fuzi and Ganjiang can protect rats with acute heart failure by enhancing mitochondrial biogenesis via Sirt1/PGC-1α signaling pathway. Hemodynamic parameters, including heart rate and left ventricular maximal rate of pressure rise and decline, were recorded in rats with acute heart failure induced by Propafenone hydrochloride. The serum levels of cardiac enzymes, including creatine kinase, lactate dehydrogenase, brain natriuretic peptide and cardiac troponin T, were also determined. The gene and protein levels of Sirtuin 1 (Sirt1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and their downstream transcription factors were measured as well. The results indicated that Fuzi-Ganjiang herbal couple provided more significant benefits by restoring the left ventricular function and cardiac enzyme activities in comparison with their single use. Moreover, this herbal couple possessed a significant cardio-protection by increasing both gene and protein levels of Sirt1 and PGC-1α. In conclusion, the compatibility of Fuzi and Ganjiang had better therapeutic effect than their single use against failing heart, and the underlying mechanisms were partially through increasing mitochondrial biogenesis via Sirt1/PGC-1α pathway.
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