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

机译:观心康汤部分通过抑制内质网应激发挥其抗动脉粥样硬化作用

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摘要

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.
机译:目的。研究冠心康(GXK)汤对高半胱氨酸血症(HCY)预处理的人脐静脉内皮细胞(HUVEC)的凋亡,线粒体膜电位(MMP)和内质网应激(ERS)的抗动脉粥样硬化作用。材料和方法。 HUVEC随机分为5组:(1)空白对照组(对照组),(2)模型对照组(模型),(3)GXK低剂量组,(4)GXK中剂量组和(5)GXK高剂量组剂量组。对于三个GXK组,在将HUVEC与含GXK的兔血清温育2小时后,给予HCY浓度达到3.0 / mmol / L。 HCY与细胞孵育后3、6、12和24 andh,收集HUVEC进行细胞凋亡率,MMP和GRP78蛋白(反映ERS)的测试。结果。在模型对照组中,与空白对照组相比,HUVEC的凋亡率和GRP 78蛋白表达显着增加(P <0.05),而MMP显着降低(P <0.05)。与模型对照组相比,中,高剂量GXK治疗后,细胞凋亡率和GRP 78蛋白表达显着下降(P <0.05),而MMP显着上升(P <0.05)。结论。 GXK可拮抗HCY引起的HUVEC损伤,其拮抗作用随浓度和治疗时间的延长而增强,其可能的作用机制可能是抑制HCY引起的ERS。

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