叔丁基对苯二酚对大鼠脑缺血再灌注损伤的保护作用及机制研究

Effect of Tert-Butylhydroquinone against cerebral ischemia reperfusion-induced brain injury

目的:探讨叔丁基对苯二酚在大鼠脑缺血再灌注中的神经保护作用及可能机制。方法:将SD雄性大鼠随机分为假手术组、缺血再灌注组、缺血再灌注加溶剂治疗组、缺血再灌注加叔丁基对苯二酚治疗组,分别于再灌注后24 h对大鼠进行行为学评分,采用免疫印迹法检测叔丁基对苯二酚对Nrf2蛋白表达的影响,TUNEL法检测神经细胞的凋亡,酶联免疫吸附法检测炎性因子TNF-α和IL-1β的表达,同时检测超氧化物歧化酶和丙二醛的含量。结果:与假手术组相比,叔丁基对苯二酚可以显著上调Nrf2蛋白的表达(P<0.05)和SOD的活性(P<0.05),显著减少MDA的表达量(P<0.05),抑制TNF-α和IL-1β的表达量(P<0.05)。结论:叔丁基对苯二酚可以在大鼠脑缺血再灌注损伤中发挥显著地神经保护作用,其机制可能与上调Nrf2信号通路相关。

Objective： To investigate the neuroprotoctive effect of Tert-Butylhydroquinone on cerebral ischemia-reperfusion（ I/R） injury. Methods： Male Sprague-Dawley rats were randomly divided into sham,I / R,I / R ＋vehicle group and I / R ＋Tert-Butylhydroquinone treatment groups. Tert-Butylhydroquinone injection was injected intraperitoneally in the rats after I / R. Neurologic deficit,histopathology changes,oxidative stress and inflammation markers were evaluated after 24 hours of reperfusion. Results： The degree of neurological deficit in the Tert-Butylhydroquinone treatment group were significantly improved compared to the vehicle treatment group. Moreover,expression of Nrf2 and SOD was increased by Tert-Butylhydroquinone treatment compared with vehicle treated sham operated control group（ P〈0. 05）. Intraperitoneal injection of Tert-Butylhydroquinone significantly decreased the expression of MDA,TNF-α,IL-1β and the number of TUNEL positive cells in rats brain after I / R（ P〈0. 05）. Conclusion： Taken together,these results suggested that Tert-Butylhydroquinone treatment effectively ameliorates the cerebral ischemia / reperfusion induced brain injury by modulating Nrf2 signaling pathway.