雷公藤红素通过抑制氧化应激对脑缺血再灌注损伤的保护研究

Protective effect of tripterine on cerebral ischemia-reperfusion injury by inhibiting oxidative stress

目的:研究雷公藤红素(Celastrol,Cel)在大鼠局灶性脑缺血再灌注(Ischemia/Reperfusion,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,腹腔注射Cel。栓塞2 h,再灌注24 h后,测定大鼠脑组织和外周血清谷胱苷肽过氧化物酶(Glutathione peroxidase,GSH-Px)、超氧化物歧化酶(Superoxide dismutase,SOD)的活性及丙二醛(Malondialdehyde,MDA)的含量。脑组织做TTC(2,3,5-氯化三苯基四氮唑)染色,检测各组脑梗死范围。结果:与模型组相比,Cel治疗组脑梗死范围均减小;组织及血清MDA(P <0. 01; P <0. 001,P <0. 01)含量降低,SOD(P <0. 01)和GSH-Px(P <0. 001; P <0. 05)的活性显著升高。结论:Cel对脑I/R损伤具有保护作用,其机制可能与Cel提高抗氧化能力,抑制I/R损伤引起的氧化应激有关。

Objective： To explore the anti-oxidation effect of Celastrol（Cel）on cerebral ischemia/reperfusion（I/R） injury. Methods： A model of middle cerebral artery occlusion was used. Ten minutes after embolization, Cel was injected intraperitoneally. The activity of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px） and malondialdehyde （MDA） in rat brain tissue and peripheral blood were measured after embolization for 2 h and reperfusion for 24 h. The range of cerebral infarction was detected by 2,3,5triphenyl four azole nitrogen chloride（TTC）. Results： Compared with the model group, the range of cerebral infarction was decreased in the Cel-treated group; the MDA of tissues and serum （ P 〈0.01; P 〈0.001, P 〈0.01）, SOD （ P 〈0.01） and GSH-Px （ P 〈0.001; P 〈0.05） was significantly increased. Conclusion： Cel has a protective effect on brain I/R injury, and its mechanism may be related to the increase of antioxidant capacity of Cel and the inhibition of oxidative stress caused by I/R injury.