依达拉奉对LPC所致兔胸主动脉内皮功能的影响及机制

目的探讨依达拉奉(edaravone,Eda)对溶血磷脂酰胆碱(lysophosphatidylcholine,LPC)所致家兔血管内皮损伤的影响及机制。方法家兔胸主动脉环分别与LPC(5 mg.L-1)和Eda(25～100μmol.L-1)单独孵育或共孵育,分别检测乙酰胆碱诱导的内皮依赖性舒张反应和硝普钠诱导的非内皮依赖性舒张反应,血管组织中一氧化氮(nitric oxide,NO)和丙二醛(malonaldehyde,MDA)含量以及超氧化物歧化酶(superoxide dismutase,SOD)的活性。结果 5 mg.L-1LPC孵育血管环30 min,明显抑制了乙酰胆碱诱导的内皮依赖性舒张反应,但没有影响硝普钠诱导的非内皮依赖性舒张反应,降低了血管组织中NO含量和SOD活性而增加了MDA含量。25～100μmol.L-1Eda分别孵育血管环15min,再与5 mg.L-1LPC共同孵育30 min,明显改善LPC所致的血管舒张功能的损害,升高了血管组织中NO含量和SOD活性而降低了MDA含量。结论 Eda对LPC所致的血管内皮依赖性舒张功能的损伤具有明显的保护作用,该效应可能与其抗氧化作用有关。

Effect of edaravone on LPC-induced vascular endothelial function in rabbit thoracic aorta and its mechanism

Aim To investigate the effect of edaravone(Eda) on damage of vascular endothelium induced by lysophosphatidylcholine(LPC) in rabbit aorta and its mechanism.Methods The endothelium-dependent relaxation response to acetylcholine and endothelium-independent relaxation response to sodium nitroprusside of aortic rings were measured by recording isometric tension after the rings were exposed to LPC(5 mg·L-1)in the absence or presence of Eda(25~100 μmol·L-1)to estimate injury effect of LPC and the protective effect of Eda on aortic endothelium,respectively.Furthermore,the content of nitric oxide(NO)and malonaldehyde(MDA),and the activity of superoxide dismutase(SOD)in the thoracic aorta rings were measured after tension test.Results Exposure of aortic rings to LPC(5 mg·L-1) for 30 min induced a significant inhibition of endothelium-dependent relaxation to acetylcholine,but did not affect endothelium-independent relaxation to sodium nitroprusside.Pre-incubation of aortic rings with Eda for 15 min and then co-incubation of the rings with LPC(5 mg·L-1) for another 30 min significantly attenuated the inhibition of endothelium-dependent relaxation induced by LPC.LPC markedly decreased the activity of SOD and the level NO but significantly increased the content of MDA in vascular tissues.However,Eda significantly increased the level of NO and the activity of SOD but significantly decreased the content of MDA in vascular tissues.Conclusion Eda may protect endothelium from being damaged by LPC.The mechanism of Eda may be related to its antioxidant defenses.