目的研究津力达联合通心络对高糖诱导胰岛微血管内皮细胞( MS-1)损伤的干预作用,并初步探讨其机制。方法通过MTS法检测细胞存活率筛选药物作用浓度；将细胞分为正常组( Normal)、模型组( Model)、津力达组( JLD)、通心络组(TXL)及津力达+通心络组(JLD+TXL),运用高n 糖(50 mmol·L-1)培养基建立损伤模型并给予药物干预, MTS法分别检测药物干预48 h、1周、2周后细胞存活率,测定给药48 h细胞上清中一氧化氮(NO)、内皮素-1(ET-1)、超氧化物歧化酶( SOD)及丙二醛( MDA)含量,流式细胞仪检测细胞活性氧簇( ROS)水平。结果首先确定 JLD 200 mg·L-1、TXL 100 mg·L-1作为给药浓度。与模型组比较,给药组升高48 h、1周、2周细胞存活率及细胞上清中NO含量(P<0．05,P<0．01),JLD、JLD+TXL组细胞上清液ET-1含量降低(P<0．05,P<0．01),JLD组细胞上清液SOD含量升高(P<0．05),JLD+TXL组细胞上清液MDA含量降低(P<0．05)；给药组细胞内 ROS 水平均降低(P <0．05,P <0．01)。结论津力达联合通心络能够改善高糖诱导MS-1细胞内皮功能损伤,并通过减轻氧化应激损伤发挥细胞保护作用。%Aim To investigate the effect of Jinlida combined with Tongxinluo on high glucose-induced en-dothelial cells ( MS-1 ) injury of islet microvessels and the possible mechanism. Methods Drug concentra-tions were defined by detecting cell viability by MTS assay. Cells were divided into normal group ( Nor-mal), model group (Model), Jinlida group (JLD), Tongxinluo group ( TXL ) and Jinlida + Tongxinluo group ( JLD + TXL ) . High glucose medium ( 50 mmol·L-1) was used to develop model, then drug in-tervention was given. Cell survival rate was detected by MTS assay after drug intervention for 48 h, 1 w and 2 w respectively. The content of nitric oxide ( NO) , en-dothelin -1 (ET-1), superoxide dismutase (SOD) and malondialdehyde ( MDA ) in cell supernatant was measured 48 h after drug intervention. ROS levels of cells were detected by flow cytometry. Results JLD 200 mg·L-1,TXL 100 mg·L-1 were defined as ad- n ministration concentration. Compared with model group, cell viability in 48 h, 1 w, 2w and NO content of cell supernatant in treatment group were significantly increased(P<0. 05, P<0. 01). ET-1 of supernatant in JLD, JLD + TXL group was significantly decreased ( P<0. 05 , P<0. 01 ) , SOD content in JLD group was significantly increased ( P<0. 05 ) , and MDA content in JLD + TXL group was significantly decreased ( P<0. 05 );ROS levels in treatment group were significant-ly decreased ( P <0. 05 , P <0. 01 ) . Conclusion Jinlida combined with Tongxinluo could improve high glucose-induced endothelial disfunction in MS-1 cells, and plays a protective role by reducing oxidative stress damage in the cells.
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