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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 7517358, 10 pages
Research Article

Astragalus Granule Prevents Ca2+ Current Remodeling in Heart Failure by the Downregulation of CaMKII

1Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China
2Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China
3Department of Medicine, Institute of Molecular Cardiology, University of Louisville, Louisville, KY 40292, USA
4Experimental Research Center, China Academy of Chinese Medical Sciences, Beijing 100700, China
5College of Basic Medicine, Beijing University of Chinese Medicine, Beijing 100029, China

Correspondence should be addressed to Yibing Nong; ude.ellivsiuol@gnon.gnibiy and Qian Lin; moc.621@26naiqnil

Received 26 May 2017; Accepted 6 July 2017; Published 10 August 2017

Academic Editor: Manel Santafe

Copyright © 2017 Sinai Li 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.


Background. Astragalus was broadly used for treating heart failure (HF) and arrhythmias in East Asia for thousands of years. Astragalus granule (AG), extracted from Astragalus, shows beneficial effect on the treatment of HF in clinical research. We hypothesized that administration of AG prevents the remodeling of L-type Ca2+ current () in HF mice by the downregulation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). Methods. HF mice were induced by thoracic aortic constriction (TAC). After 4 weeks of AG treatment, cardiac function and QT interval were evaluated. Single cardiac ventricular myocyte was then isolated and whole-cell patch clamp was used to record action potential (AP) and . The expressions of L-type calcium channel alpha 1C subunit (Cav1.2), CaMKII, and phosphorylated protein kinase A (p-PKA) were examined by western blot. Results. The failing heart manifested distinct electrical remodeling including prolonged repolarization time and altered kinetics. AG treatment attenuated this electrical remodeling, supported by AG-related shortened repolarization time, decreased peak , accelerated inactivation, and positive frequency-dependent facilitation. In addition, AG treatment suppressed the overexpression of CaMKII, but not p-PKA, in the failing heart. Conclusion. AG treatment protected the failing heart against electrical remodeling and remodeling by downregulating CaMKII.