三七皂苷R1对氧化型低密度脂蛋白诱导血管内皮细胞凋亡的保护作用  

Notoginsenoside R1 protects vascular endothelial cells from ox-LDL-induced apoptosis

作　　者：孟伟阳 李永领 闻浩 潘达 陈健 金灿 叶孙志 陈大庆 MENG Weiyang;LI Yongling;WEN Hao;PAN Da;CHEN Jian;JIN Can;YE Sunzhi;CHEN Daqing(Department of Emergency Medicine,the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University,Wenzhou 325027,China)

机构地区：[1]温州医科大学附属第二医院、育英儿童医院急诊医学科,315027

出　　处：《浙江医学》2021年第7期711-715,I0007,共6页Zhejiang Medical Journal

摘　　要：目的探讨三七皂苷R1(NGR1)对氧化型低密度脂蛋白(ox-LDL)诱导血管内皮细胞凋亡的保护作用及其机制。方法将体外培养人脐静脉内皮细胞(HUVECs)分为对照组、损伤组(ox-LDL组)和4种浓度NGR1治疗组(ox-LDL+不同浓度NGR1组);采用CCK-8法检测NGR1的药物毒性以及各组HUVECs的增殖活性,采用Western blot法检测Bcl-2、Bax及Cleaved-caspase-3凋亡相关蛋白表达情况,免疫荧光染色检测Cleaved-caspase-3凋亡情况,钙黄绿素细胞膜标记染色检测细胞黏附能力,Trans well迁移试验检测细胞迁移能力。结果与对照组比较,损伤组HUVECs的凋亡率和Cleaved-caspase-3表达水平显著升高,并且HUVECs的增殖活性、细胞黏附能力和迁移能力均显著降低(均P<0.05)。与损伤组比较,NGR1治疗组HUVECs的凋亡率和Cleaved-caspase-3表达水平均随着NGR1浓度的增加而逐渐下降,HUVECs的增殖活性、细胞黏附能力和迁移能力均随着NGR1浓度的增加而逐渐升高(均P<0.05)。结论NGR1通过抑制ox-LDL诱导的HUVECs细胞增殖活性降低、Cleaved-caspase-3表达上调而引起的细胞凋亡增多、细胞黏附和迁移数量减少,从而发挥其对ox-LDL损伤的血管内皮细胞的保护作用。Objective To investigate the effect of notoginsenoside Rl(NGRl)on oxidized low-densitylipoprote in(ox-LDL)-induced apoptosis of vascular endothelial cells and its mechanism.Methods Human umbilical vein endothelial cells(HUVECs)were divided into control group,injury group(ox-LDL stimulation)and NGR1 treatment groups(ox-LDL+NGR1 treatment with various concentrations).CCK-8 was used to detect the toxicity of NGRl and prolife ration of HUVEC s,Western blot for expression of Bc1-2,Bax,Cleared-caspase-3 and immunofluorescence staining for expression of Cleared-caspase-3 were used to detected the apoptosis of HUVECs,calcein AM staining of cell membrane was used to detect the adhesion ability of HUVECs to extracellular matrix,Transwell test was used to detect the migration ability of HUVECs.Results Compared with control group,the apoptosis rate of HUVECs and the expression level of Cleaved-caspase-3 protein in the injury group were significantly inc reased,and the prolife ration ability,cell adhesion ability and migration effiiency of HUVECs were significantlyreduced(P<0.05).Compared with the injury group,the apoptosis rate of HUVECs and the expression level of Cleaved-caspase-3 protein in the NGR1 treatment groups decreased with the increase of the NGR1 concentration,and the prolife ration ab ility,cell adhesion ability and migration ability of HUVECs were increased with the increase of NGR1 concentration(P<0.05).Conclusion NGR1 protects vascular endothelial cells from ox-LDL-induced injury through enhancing cell proliferation ability,inhibiting cell apoptosis,and increasing cell adhesion and migration.

关 键 词：三七皂苷R1 人脐静脉内皮细胞 细胞凋亡 细胞黏附 细胞迁移 

分 类 号：R285[医药卫生—中药学]