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Evid Based Complement Alternat Med. 2017;2017:7517358. doi: 10.1155/2017/7517358. Epub 2017 Aug 10.

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

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



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 (ICa-L) in HF mice by the downregulation of Ca2+/calmodulin-dependent protein kinase II (CaMKII).


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 ICa-L. 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.


The failing heart manifested distinct electrical remodeling including prolonged repolarization time and altered ICa-L kinetics. AG treatment attenuated this electrical remodeling, supported by AG-related shortened repolarization time, decreased peak ICa-L, accelerated ICa-L inactivation, and positive frequency-dependent ICa-L facilitation. In addition, AG treatment suppressed the overexpression of CaMKII, but not p-PKA, in the failing heart.


AG treatment protected the failing heart against electrical remodeling and ICa-L remodeling by downregulating CaMKII.

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