川芎嗪肉桂酰类双酯衍生物对内皮细胞氧化损伤的保护作用

Protective Effects of 2,5-bis(2,5-dimethoxy-cinnamoyoxymethyl)-3,6 -Dimethyl Pyrazine on Endothelial Cells Injured by Hydrogen Peroxide

目的观察2,5-二(2,5-二甲氧基肉桂酰氧甲基)-3,6-二甲基吡嗪(TMPC)对H_2O_2引起的体外培养人脐静脉内皮细胞氧化性损伤的保护作用,并初步探讨其作用机制。方法 H_2O_2引起体外培养人脐静脉内皮细胞氧化性损伤,观察TMPC对内皮细胞氧化损伤的保护作用。结果 TMPC对H_2O_2引起体外培养人脐静脉内皮细胞氧化性损伤有明显的保护作用,能减少内皮细胞脂质过氧化物丙二醛(Malondialdehyde,MDA)的生成,提高超氧化物歧化酶(SOD)活性,减轻H_2O_2诱导的内皮细胞内游离钙离子升高引起的钙超载。结论 TMPC可有效保护H_2O_2引起体外培养人脐静脉内皮细胞氧化性损伤,维持或恢复细胞正常的生理功能,其机制可能与TMPC能有效抑制细胞内钙超载,减少脂质过氧化物的生成,提高抗氧化物质的活性有关。

Objective To investigate the protection of 2,5-bis （ 2, 5-dimethoxy-cinnamoyoxymethyl ） -3,6-dimethylpyrazine （ TMPC ） on oxidative damage to human umbilical vein endothelial cells （ HUVECs ）. Methods The HUVECs were damaged by hydrogen peroxide{ H202）, the protective effect of TMPC on endothelial cells was observed. Results TMPC protected the injured cells obviously, dcreased the malondialdehyde （ MDA } level induced by oxidative damage, increased the activity of superoxide disutase （ SOD ） , and reduced the calcium overload caused by the free calcium-induced in the oxidative damaged endothelial ceils. Conclusion TMPC has potent protection on oxidative damage,its potential mechanism relates to inhibiting the intracellular calcium overload and suppressing the generation of reactive oxygen species.