枸杞多糖减轻ox-LDL诱导血管内皮细胞损伤的效应及分子机制研究

Effects of Lyciumbarbarum polysaccharide ameliorating ox-LDL-induced vascular endothelial cell injury and its molecular mechanism

目的:研究枸杞多糖(LBP)减轻氧化型低密度脂蛋白(ox-LDL)诱导血管内皮细胞损伤的效应及分子机制。方法:培养人脐静脉内皮细胞(HUVECs)并分为对照组(不含药物的DMEM处理)、ox-LDL组(含有150 mg/L ox-LDL的DMEM处理)、LBP组(含有150 mg/L ox-LDL及100 mg/L LBP的DMEM处理)、LBP+LY组(含有150 mg/L ox-LDL、100 mg/L LBP、20μmol/L LY294002的DMEM处理)。检测细胞活力、凋亡率、线粒体凋亡基因及PI3K/AKT通路基因的表达量。结果:ox-LDL组的细胞活力及细胞中Bcl-2、p-PI3K、p-AKT的表达量明显低于对照组,凋亡率及细胞中Bax、Caspase-3的表达量明显高于对照组(P<0.05);LBP组的细胞活力及细胞中Bcl-2、p-PI3K、p-AKT的表达量明显高于ox-LDL组,凋亡率及细胞中Bax、Caspase-3的表达量明显低于ox-LDL组(P<0.05);LBP+LY组的细胞活力及细胞中Bcl-2、p-PI3K、p-AKT的表达量明显低于LBP组,凋亡率及细胞中Bax、Caspase-3的表达量明显高于LBP组(P<0.05)。结论:LBP能够通过激活PI3K/AKT通路减轻ox-LDL诱导的血管内皮细胞损伤。

Objective:To study the effects and molecular mechanism of Lyciumbarbarum polysaccharide(LBP)ameliorating oxidized low density lipoprotein(ox-LDL)induced vascular endothelial cell injury.Methods:Human umbilical vein endothelial cells(HUVECs)were cultured and divided into control group(DMEM treatment without drugs),ox-LDL group(DMEM treatment with 150 mg/L ox-LDL),LBP group(DMEM treatment with 150 mg/L ox-LDL and 100 mg/L LBP),and LBP+LY group(DMEM treatment with 150 mg/L ox-LDL,100 mg/L LBP,20μmol/L LY294002).The cell viability,apoptotic rate,mitochondrial apoptotic gene expression and PI3K/AKT pathway gene expression were detected.Results:The cell viability and the expression of Bcl-2,p-PI3K and p-AKT in ox-LDL group were significantly lower than those in control group,the apoptotic rate and the expression of Bax and Caspase-3 in cells were significantly higher than those in control group(P<0.05).The cell viability and the expression of Bcl-2,p-PI3K and p-AKT in LBP group were significantly higher than those in ox-LDL group,the apoptotic rate and the expression of Bax and Caspase-3 in cells were significantly lower than those in ox-LDL group(P<0.05).The cell viability and the expression of Bcl-2,p-PI3K and p-AKT in LBP+LY group were significantly lower than those in LBP group,the apoptotic rate and the expression of Bax and Caspase-3 in cells of LBP+LY group were significantly higher than those in LBP group(P<0.05).Conclusion:LBP can ameliorate ox-LDL induced vascular endothelial cells injury by activating PI3K/AKT pathway.