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目的探讨黑果枸杞花色苷对体外氧化低密度脂蛋白(ox-LDL)所致人脐静脉内皮细胞(HUVECs)氧化损伤的保护作用。方法利用体外培养人脐静脉血管内皮细胞,建立了氧化低密度脂蛋白氧化损伤模型。将细胞分为6组:正常组、氧化低密度脂蛋白组、辛伐他汀组、花色苷低剂量+氧化低密度脂蛋白组,花色苷中剂量+氧化低密度脂蛋白组和花色苷高剂量+氧化低密度脂蛋白组。各剂量组经实验处理后进行细胞计数及形态观察,利用四甲基偶氮唑盐(MTT)比色法检测细胞增殖能力,运用流式细胞术(FCM)检测内皮细胞增殖周期及凋亡率,并对细胞代谢中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、过氧化物酶(POD)的活性进行检测。结果中高浓度的花色苷可以有效的抑制氧化低密度脂蛋白对血管内皮细胞的损伤,减缓被损伤细胞的G0/G1比率及凋亡率,增高S期细胞比率、G2/M比率;同时提高细胞代谢中超氧化物歧化酶、过氧化物酶、谷胱甘肽过氧化酶的活性,降低丙二醛的含量。结论黑果枸杞花色苷对氧化低密度脂蛋白所损伤的人脐静脉内皮细胞具有保护作用,其机制可能与抗氧化作用有关。
Objective To investigate the protective effects of anthocyanins from Lycium barbarum on oxidative damage of human umbilical vein endothelial cells (HUVECs) induced by oxidized low density lipoprotein (ox-LDL) in vitro. Methods Human umbilical vein endothelial cells were cultured in vitro to establish an oxidative low density lipoprotein oxidative injury model. The cells were divided into 6 groups: normal group, low density lipoprotein oxidized group, simvastatin group, low dose of anthocyanin + low density lipoprotein group, middle dose of anthocyanin + low density lipoprotein group and high dose of anthocyanin + Oxidized low density lipoprotein group. The cell counts and morphological changes were observed after treatment in each dose group. Cell proliferation was detected by MTT colorimetric assay. The proliferation and apoptosis of endothelial cells were detected by flow cytometry (FCM) , And the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and peroxidase (POD) in cell metabolism were detected. Results High concentrations of anthocyanins could effectively inhibit the damage of vascular endothelial cells by oxidized low density lipoprotein, slow down the G0 / G1 ratio and apoptosis rate of injured cells, increase the ratio of S phase cells and G2 / M ratio, Metabolism superoxide dismutase, peroxidase, glutathione peroxidase activity, reduce the content of malondialdehyde. Conclusion Anthracnose of Lycium barbarum has a protective effect on human umbilical vein endothelial cells injured by oxidized low-density lipoprotein, and its mechanism may be related to the anti-oxidation effect.