摘要
目的:观察血管紧张素转换酶抑制剂(angiotensin-converting enzyme inhibitor,ACEI)卡托普利、中药黄芪以及两者合用对损伤HUVEC的保护作用,并探讨其机制。方法:将HUVEC分为:(1)正常对照组;(2)H2O2损伤对照组;(3)卡托普利和黄芪单用低、中、高浓度组;(4)卡托普利与黄芪合用低、中、高浓度组。收集细胞,测定各组细胞活力(MTT)、抗氧化指标(MDA、SOD、NO等)以及VEGF蛋白含量。结果:除黄芪低浓度组外(P>0.05),正常对照组、卡托普利各浓度组、黄芪中高浓度组及合用组分别与H2O2损伤对照组比较,细胞活力(MTT)、SOD活性以及NO含量均显著升高(P<0.05),MDA含量显著降低(P<0.05)。卡托普利、黄芪低、中、高浓度联合与单独作用比较,MDA含量降低,MTT(OD)、SOD活性、NO含量以及VEGF蛋白含量升高,均具有统计学意义(P<0.05)。结论:卡托普利、黄芪对氧化损伤HUVEC具有保护作用,可提高其活力,增强SOD活性,增加NO和VEGF含量,降低MDA含量,呈现一定的浓度依赖性,而相同浓度的两药联合应用时保护作用更明显。
AIM: To investigate the protective effects and mechanisms of captopril or / and Milkvetch root on human umbilical vascular endothelial cells( HUVECs) with the damage of hydrogen peroxide( H2O2). METHODS: HUVECs were divided into control group,H2O2 group,captopril-L,M,H groups,Milkvetch root-L,M,H groups and captopril-L, M, H + Milkvetch root-L, M, H groups. The activity( MTT),antioxidabt indicatrix( MDA,SOD and NO) and the content of VEGF of cells were measured. RESULTS: The level of MTT( OD),the activity of SOD,the content of NO and VEGF of cells in the control and( captopril-L,M,H / Milkvetch root-M,H) groups were significantly higher than those in the H2O2group( P〈0. 05) except for Milkvetch root-L group( P〈0. 05). Besides the content of MDA of cells in the control group and( captopril-L,M,H / Milkvetch root-M,H) groups were significantly lower than those in the H2O2group( P〈0. 05) except for Milkvetch root-L + H2O2group( P〈0. 05),the effects of MTT,SOD,NO and VEGF in( captopril + Milkvetch root)-L,M,H groups were significantly better than those in the captopril / Milkvetch root-L,M,H groups( P〈0. 05). CONCLUSION: Captopril and Milkvetch root can pretect HUVECs injuried by H2O2. They can improve the cell activity( MTT),enhance the activity of SOD, increase the level of NO and VEGF,and decrease the content of MDA depending on their concentration in some extent. The combined effect of captopril and Milkvetch root is better than the independent effect of them.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2015年第8期891-895,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics