小檗碱改善高糖诱导血管内皮细胞和微血管内皮细胞损伤

摘要

目的:探讨小檗碱对高糖引起的人脐静脉血管内皮细胞(HUVEC)和人心脏微血管内皮细胞(HC-MEC)损伤的保护作用.方法:采用含5mM葡萄糖的完全培养基培养的HUVEC和HCMEC为对照组;含30、50、100、200mM葡萄糖的完全培养基培养的HUVEC和HCMEC为各高糖组;含100mM葡萄糖和0. 01、0. 1、1μM小檗碱的完全培养基培养的HUVEC和HCMEC为各小檗碱组,各组处理24h和48h后应用MTT法检测细胞活力.应用诱导型一氧化氮合酶(iNOS)试剂盒检测HUVEC细胞iNOS活性.结果:与对照组比较,30、50、100、200 mM葡萄糖浓度依赖性引起HUVEC和HCMEC的细胞活力依次下降(P<0. 05).同组细胞处理48h与24h比较,随着作用时间的延长细胞活力降低越明显.0. 01μM、0. 1μM和1μM小檗碱组较l00mM高糖组细胞活力在一定程度上有所改善(P<0. 05).与对照组比较,高糖组HUVEC的iNOS活性增加(P<0. 01),小檗碱组较高糖组iNOS活性明显降低(P<0. 01).结论:30-200 mM高糖可造成HUVEC和HCMEC损伤,小檗碱对损伤有一定的保护作用,其作用和下调iNOS活性有关.%Objective: To investigate the ameliorative effects of berberine on high glucose-induced damage of human umbilical vein endothelial cells (HUVEC) and human cardiac microvascular endothelial cells (HCMEC). Method: HUVEC and HCMEC were cultured in complete medium containing 5 mM glucose as control group, HU-VEC and HCMEC were cultured in complete medium containing 30, 50, 100 and 200 mM glucose for each high glucose group. HUVEC and HCMEC were cultured in complete medium containing 100 mM glucose and 0. 01, 0. 1, 1 μM berberine were each berberine group. After 24h and 48h treatment, the cell viability was measured by MTT assay. The iNOS activity of HUVEC was detected by inducible nitric oxide synthase (iNOS) kit. Results: Compared with control group, 30, 50, 100 and 200mM glucose induced HUVEC and HCMEC cell viability decreased in a dose-dependent manner(P<0. 05). Compared with 24h in the same group, the cell viability decreased with the prolongation of the time. The cell viability of 0. 01μM, 0. 1μM and 1μM berberine group was improved to some extent compared with 100 mM high glucose group (P<0. 05). Compared with the control group, the iNOS activity of HUVEC in l00mM glucose group was increased (P<0. 01), and the activity of iNOS in berberine group was significantly lower than that in high glucose group (P<0. 01). Conclusion: High glucose can cause HUVEC and HCMEC damage in 30 - 200mM. Berberine has a protective effect on the damage, and its cffect is related to down-regulation of iNOS activity.