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目的观察PPARγ激动剂对大鼠局灶性脑缺血再灌注损伤(I/R)的保护作用,并对其作用机制进行初步探讨。方法复制大鼠大脑中动脉阻塞再灌注模型(MCAO/R),分别采用TTC染色法、神经功能缺损评分法观察PPARγ激动剂对大鼠脑梗死体积和行为学评分的影响,同时观察PPARγ激动剂对脑组织形态学和丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性、诱导型一氧化氮合酶(iNOS)活化和一氧化氮(NO)含量的影响。结果PPARγ激动剂能够降低I/R大鼠脑梗死体积和行为学评分,减轻受损大鼠皮层脑组织的病理改变,抑制脑组织中MDA的生成、提高SOD的活性、抑制iNOS活性、降低NO含量。结论PPARγ激动剂对大鼠脑缺血再灌注损伤有一定保护作用,其作用机制与增强SOD活性,抑制脑组织中iNOS活性、降低NO和MDA含量及减轻I/R中氧化损伤有关。
Objective To observe the protective effect of PPARγ agonist on focal cerebral ischemia-reperfusion injury (I / R) in rats and its mechanism of action. Methods Rat middle cerebral artery occlusion / reperfusion (MCAO / R) model was established. The effects of PPARγ agonist on cerebral infarction volume and behavioral score were observed by TTC staining and neurological deficit score. The effects of PPARγ agonist On the histomorphology and the level of malondialdehyde (MDA), the activity of superoxide dismutase (SOD), the activity of inducible nitric oxide synthase (iNOS) and the content of nitric oxide (NO) in brain tissue. Results The PPARγ agonist could decrease the volume and behavior of cerebral infarction in I / R rats, alleviate the pathological changes of cortex in rats, inhibit the production of MDA, increase the activity of SOD, inhibit the activity of iNOS and decrease the NO content. Conclusions PPARγ agonist may protect rats from cerebral ischemia-reperfusion injury. Its mechanism may be related to the increase of SOD activity, inhibition of iNOS activity in brain tissue, reduction of NO and MDA content, and reduction of oxidative damage in I / R.