津力达联合通心络对高糖诱导胰岛微血管内皮细胞损伤干预作用及机制研究  

Effect of Jinlida combined with Tongxinluo on high glucose-induced endothelial cells injury of islet microvessels

作　　者：庞洁 梁俊清 王志鑫 魏聪 高怀林[3,4] 

机构地区：[1]河北以岭医药研究院 [2]国家中医药管理局重点研究室(心脑血管络病) [3]河北省络病重点实验室 [4]河北医科大学附属以岭医院(国家中医药管理局中医络病学重点学科),河北石家庄050035

出　　处：《中国药理学通报》2015年第3期430-435,共6页Chinese Pharmacological Bulletin

基　　金：国家重点基础研究发展计划(973计划)资助项目(No2012CB518606);河北省自然科学基金资助项目(No H2013106139)

摘　　要：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 200mg·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-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.

关 键 词：津力达 通心络 胰岛微血管细胞 高糖 内皮功能 氧化应激 机制 

分 类 号：R332[医药卫生—人体生理学] R322.12[医药卫生—基础医学]