【摘要】 采用过氧化氢诱导建立的内皮细胞氧化损伤模型,探讨了丹参酮ⅡA对氧化损伤的HUVECs的保护作用。通过内皮细胞LDH、SOD、NOS、GSH-Px的活性和MDA、NO含量的变化趋势,MTT和流式细胞术反映的细胞存活率的变化,研究了丹参酮ⅡA对正常和氧化损伤HUVECs的作用。结果表明丹参酮ⅡA在10～100μmol/L浓度之间时,无明显细胞毒性。浓度在20μmol/L以上时,丹参酮ⅡA能显著增强HUVECs抵御氧化损伤的能力;同时降低了LDH的泄漏,阻止了MDA等过氧化物的生成,提高了NOS、NO、SOD和GSH-PX分泌量,显著减少了细胞早期凋亡率和坏死率。表明丹参酮ⅡA可以保护HUVECs免受氧化损伤,防止动脉粥样硬化斑块的形成。更多还原

【Abstract】 The oxidative injury model established with H2O2 was used to study the protective effects of Tanshinone ⅡA on the oxidative damage of HUVECs.The activities of LDH,SOD,NOS and GSH-Px,and the contents of NO and MDA were determined in each experimental groups.The livability of HUVECs was determined by MTT assay and flow cytometry was employed to analysis the influences on the normal and the oxidative injury HUVECs.The results showed that Tanshinone ⅡA has no cytotoxicity at 10-100 μmol/L of concentration.The ability of protecting HUVECs from oxidative injury was enhanced obviously at more than 20 μmol/L of Tanshinone IIA and the releasing percentage of LDH and the content of MDA were decreased while the activity of NOS,NO,SOD and GSH-PX were increased.The apoptosis and the rate of the death were reduced significantly.Results indicated that Tanshinone ⅡA could prevent HUVECs from oxidative damage which caused the formation of atherosclerotic plaques.更多还原