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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 3197320, 11 pages
Research Article

Qiliqiangxin Enhances Cardiac Glucose Metabolism and Improves Diastolic Function in Spontaneously Hypertensive Rats

1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China
2Department of Cardiology, People’s Hospital of Nanbu County, Nanchong, Sichuan, China
3Department of Cardiology, Shandong University, Jinan, Shandong, China

Correspondence should be addressed to Jingmin Zhou; nc.hs.latipsoh-sz@nimgnij.uohz

Received 18 January 2017; Revised 8 April 2017; Accepted 7 May 2017; Published 19 June 2017

Academic Editor: Giuseppe Caminiti

Copyright © 2017 Jingfeng Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cardiac diastolic dysfunction has emerged as a growing type of heart failure. The present study aims to explore whether Qiliqiangxin (QL) can benefit cardiac diastolic function in spontaneously hypertensive rat (SHR) through enhancement of cardiac glucose metabolism. Fifteen 12-month-old male SHRs were randomly divided into QL-treated, olmesartan-treated, and saline-treated groups. Age-matched WKY rats served as normal controls. Echocardiography and histological analysis were performed. Myocardial glucose uptake was determined by 18F-FDG using small-animal PET imaging. Expressions of several crucial proteins and key enzymes related to glucose metabolism were also evaluated. As a result, QL improved cardiac diastolic function in SHRs, as evidenced by increased and decreased (). Meanwhile, QL alleviated myocardial hypertrophy, collagen deposits, and apoptosis (). An even higher myocardial glucose uptake was illustrated in QL-treated SHR group (). Moreover, an increased CS activity and ATP production was observed in QL-treated SHRs (). QL enhanced cardiac glucose utilization and oxidative phosphorylation in SHRs by upregulating AMPK/PGC-1α axis, promoting GLUT-4 expression, and regulating key enzymes related to glucose aerobic oxidation such as HK2, PDK4, and CS (). Our data suggests that QL improves cardiac diastolic function in SHRs, which may be associated with enhancement of myocardial glucose metabolism.