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Evidence-Based Complementary and Alternative Medicine
Volume 2014, Article ID 465640, 8 pages
Research Article

Guanxinkang Decoction Exerts Its Antiatherosclerotic Effect Partly through Inhibiting the Endoplasmic Reticulum Stress

1Department of Traditional Chinese Medicine, The First Hospital of Shijiazhuang City, 36 Fanxi Road, Shijiazhuang, Hebei 050011, China
2First Hospital of Shijiazhuang and Organ Transplantation Committee in Chinese Medical Association, 36 Fanxi Road, Shijiazhuang, Hebei 050011, China

Received 7 November 2013; Revised 10 March 2014; Accepted 10 March 2014; Published 18 May 2014

Academic Editor: Joen-Rong Sheu

Copyright © 2014 Hao 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.


Purpose. To investigate the antiatherosclerotic effect of Guanxinkang (GXK) decoction on the apoptosis, mitochondrial membrane potential (MMP), and endoplasmic reticulum stress (ERS) of human umbilical vein endothelial cells (HUVEC) pretreated with homocysteinemia (HCY). Materials and Methods. HUVEC were randomly divided into 5 groups: (1) blank control group (control), (2) model control group (model), (3) GXK low dose group, (4) GXK medium dose group, and (5) GXK high dose group. For the three GXK groups, HCY was given to reach the concentration of 3.0 mmol/L after HUVEC had been incubated with rabbit serum containing GXK for two hours. At 3, 6, 12, and 24 h after HCY had been incubated with the cells, the HUVEC were collected for test of the apoptosis rate, MMP, and GRP78 protein (reflecting ERS). Results. In the model control group, the apoptosis rate and GRP 78 protein expression of HUVEC significantly increased ( ), while MMP significantly decreased ( ) compared with the blank control group. After GXK treatment of medium and high doses, the apoptosis rate and the GRP 78 protein expression significantly ( ) decreased, while MMP significantly increased ( ) in a time-dependent manner compared with the model control group. Conclusion. GXK can antagonize the injury of HUVEC caused by HCY and the antagonism effect increases with the concentration and treatment duration of GXK, with the possible mechanism of GXK antagonism being through inhibiting ERS caused by HCY.