Wang Hao, Zheng Zhi-Min, Gao Bu-Lang
Department of Traditional Chinese Medicine, The First Hospital of Shijiazhuang City, 36 Fanxi Road, Shijiazhuang, Hebei 050011, China.
First Hospital of Shijiazhuang and Organ Transplantation Committee in Chinese Medical Association, 36 Fanxi Road, Shijiazhuang, Hebei 050011, China.
Evid Based Complement Alternat Med. 2014;2014:465640. doi: 10.1155/2014/465640. Epub 2014 May 18.
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 (P < 0.05), while MMP significantly decreased (P < 0.05) compared with the blank control group. After GXK treatment of medium and high doses, the apoptosis rate and the GRP 78 protein expression significantly (P < 0.05) decreased, while MMP significantly increased (P < 0.05) 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.
目的。探讨冠心康（GXK）水煎剂对同型半胱氨酸血症（HCY）预处理的人脐静脉内皮细胞（HUVEC）凋亡、线粒体膜电位（MMP）及内质网应激（ERS）的抗动脉粥样硬化作用。材料与方法。将HUVEC随机分为5组：（1）空白对照组（对照组），（2）模型对照组（模型组），（3）GXK低剂量组，（4）GXK中剂量组，（5）GXK高剂量组。对于3个GXK组，在HUVEC与含GXK的兔血清孵育2小时后，给予HCY使其达到3.0 mmol/L的浓度。在HCY与细胞孵育3、6、12和24小时后，收集HUVEC用于检测凋亡率、MMP和GRP78蛋白（反映ERS）。结果。与空白对照组相比，模型对照组中HUVEC的凋亡率和GRP 78蛋白表达显著增加（P < 0.05），而MMP显著降低（P < 0.05）。与模型对照组相比，中、高剂量的GXK处理后，凋亡率和GRP 78蛋白表达显著（P < 0.05）降低，而MMP显著增加（P < 0.05），且呈时间依赖性。结论。GXK可拮抗HCY对HUVEC的损伤，且拮抗作用随GXK的浓度和处理时间延长而增强，其可能的拮抗机制是通过抑制HCY引起的ERS。
