Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats | Zendy

Junfang Zhang | Zendy; Cong Wei | Zendy; Hongtao Wang | Zendy; Siwen Tang | Zendy; Zhenhua Jia | Zendy; Lei Wang | Zendy; Dengfeng Xu | Zendy; Yiling Wu | Zendy

Open Access

Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats

Author(s) -

Junfang Zhang,

Cong Wei,

Hongtao Wang,

Siwen Tang,

Zhenhua Jia,

Lei Wang,

Dengfeng Xu,

Yiling Wu

Publication year - 2013

Publication title -

evidence-based complementary and alternative medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.552

H-Index - 90

eISSN - 1741-4288

pISSN - 1741-427X

DOI - 10.1155/2013/378298

Subject(s) - pressure overload , heart failure , ampk , medicine , constriction , mitochondrion , endocrinology , cardiac function curve , cardiology , beta oxidation , chemistry , metabolism , biochemistry , protein kinase a , cardiac hypertrophy , kinase

Qiliqiangxin capsule (QL) was developed under the guidance of TCM theory of collateral disease and had been shown to be effective and safe for the treatment of heart failure. The present study explored the role of and mechanism by which the herbal compounds QL act on energy metabolism, in vivo , in pressure overload heart failure. SD rats received ascending aorta constriction (TAC) to establish a model of myocardial hypertrophy. The animals were treated orally for a period of six weeks. QL significantly inhibited cardiac hypertrophy due to ascending aortic constriction and improved hemodynamics. This effect was linked to the expression levels of the signaling factors in connection with upregulated energy and the regulation of glucose and lipid substrate metabolism and with a decrease in metabolic intermediate products and the protection of mitochondrial function. It is concluded that QL may regulate the glycolipid substrate metabolism by activating AMPK/PGC-1 α axis and reduce the accumulation of free fatty acids and lactic acid, to protect cardiac myocytes and mitochondrial function.

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