目的:研究三氟淫羊藿素(Icaritfluor,ICTF)在大鼠局灶性脑缺血再灌注(I/R)损伤中的作用。方法:采用大鼠大脑中动脉栓塞模型,栓塞后10 min,分别于腹腔注射二甲基亚砜、依达拉奉及不同浓度的ICTF。栓塞2 h,再灌注24 h后,腹主动脉取血,并分离血清,比色法检测血清超氧化物歧化酶(SOD)、谷胱苷肽过氧化物酶(GSHPx)的活性及丙二醛(MDA)、一氧化氮(NO)的含量。脑组织做TTC染色,检测各组脑梗死范围。结果:与模型组相比,ICTF治疗组脑梗死范围均减小;血清MDA(P〈0.001)和NO(P〈0.05)含量降低,SOD(P〈0.05,P〈0.01)和GSH-Px(P〈0.05)的活性显著升高。结论:ICTF对脑I/R损伤具有保护作用,其机制可能是ICTF抑制I/R损伤引起的氧化应激。
Objective: To explore the anti-oxidation effect of trifluoro-icaritin(ICTF) on cerebral ischemia/reperfusion(I/R) injury. Methods: Middle cerebral artery occlusion model was made in this experiment. The rats were treated with DMSO,3 mg·kg^-1Edaravone,1 and 2 mg·kg^-1does of ICTF by intraperitoneal injection 10 min after the ischemia.Reperfusion for 24 h,blood was got from the abdominal aorta. The serum was separated to detective the activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px),and the levels of malonaldehyde(MDA) and nitric oxide(NO); The range of cerebral infarction was detected by 2,3,5-triphenyl four azole nitrogen chloride(TTC). Results:After treating with ICTF,the rat's brain volume of infarction was reduced,the levels of MDA and NO in serum were decreased,and the activities of SOD and GSH-Px in serum were increased. Conclusion: ICTF has a neuroprotection effects on cerebral I/R injury because it inhibits oxidative stress.