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Int J Biol Sci 2011; 7(3):383-389. doi:10.7150/ijbs.7.383

Research Paper

Tanshinone IIA Protects Against Cardiac Hypertrophy via Inhibiting Calcineurin/Nfatc3 Pathway

Xueying Tan1*, Jianping Li1*, Xinyue Wang1, Nan Chen1, Benzhi Cai1, Gang Wang1, Hongli Shan1, Deli Dong1, Yanju Liu1, Xingda Li1, Fan Yang1, Xin Li1, Peng Zhang1, Xueqi Li3, Baofeng Yang1,2, Yanjie Lu1,2 ✉

1. Department of Pharmacology, State-Province Key Laboratories of Biomedicine- Pharmaceutics of China, Harbin Medical University, Harbin 150081, Heilongjiang Province, China
2. Institute of Cardiovascular Research, Harbin Medical University, Harbin 150081, Heilongjiang Province, China
3. Department of Cardiology, The Forth Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China
* The first two authors made equal contribution to this work.


Pathological cardiac hypertrophy induced by adrenergic overactivation can subsequently develop to heart failure which remains as a leading cause of mortality worldwide. Tanshinone IIA is a lipid-soluble pharmacologically active compound extracted from the rhizome of the Chinese herb Salvia miltiorrhiza, a well-known traditional Chinese medicine used for the treatment of cardiovascular disorders. However, little is know about the effect of Tanshinone IIA on cardiac hypertrophy. The present study was aimed to investigate whether Tanshinone IIA prevents cardiac hypertrophy induced by isoproterenol (ISO) and to clarify its possible mechanisms. Cardiomyocytes hypertrophy was induced by ISO 10 μM for 48 h with or without Tanshinone IIA 10, 30, 100 μM pretreatment, and evaluated by determining the cell size and the expression of ANP, BNP, β-MHC, Calcineurin, and NFATc3 by real-time PCR and western blot. We found that Tanshinone IIA pretreatment attenuated the enlargement of cell surface area induced by ISO in cultured cardiomyocytes. The mRNA level of ANP, BNP and β-MHC was obviously elevated in ISO-treated cardiac cells, which was effectively inhibited by Tanshinone IIA. Moreover, we found that Tanshinone IIA pretreatment could prevent the augment of intracellular calcium transient in ISO-treated cardiomyocytes. The further study revealed that Calcineurin, NFATc3, ANP, BNP and β-MHC proteins were upregulated by ISO in ventricular myocytes, and Tanshinone IIA pretreatment significantly attenuate the increased expression of Calcineurin, NFATc3, ANP, BNP and β-MHC proteins. In summary, Tanshinone IIA attenuated cardiomyocyte hypertrophy induced by ISO through inhibiting Calcineurin/NFATc3 pathway, which provides new insights into the pharmacological role and therapeutic mechanism of Tanshinone IIA in heart diseases.

Keywords: Tanshinone IIA, Cardiac hypertrophy, Isoproterenol, Calcineurin, NFATc3

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See for full terms and conditions.
How to cite this article:
Tan X, Li J, Wang X, Chen N, Cai B, Wang G, Shan H, Dong D, Liu Y, Li X, Yang F, Li X, Zhang P, Li X, Yang B, Lu Y. Tanshinone IIA Protects Against Cardiac Hypertrophy via Inhibiting Calcineurin/Nfatc3 Pathway. Int J Biol Sci 2011; 7(3):383-389. doi:10.7150/ijbs.7.383. Available from