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目的探讨预先电刺激小脑顶核(fastigial nucleus stimulation,FNS)启动中枢神经系统内源性神经保护对大鼠局灶脑缺血溶栓时间窗的影响,探讨PPARγ介导炎性机制在FNS对溶栓预后影响中的作用。方法将60只SD大鼠按随机数字表法分成FNS组和对照组,每组30只。FNS组预先给予电刺激小脑顶核1 h,电刺激完成后即刻制备大鼠大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型;对照组不予电刺激小脑顶核,仅制备MCAO模型。分别于栓塞后1、3、6、9、12、15 h溶栓;溶栓后72 h予以神经功能评分后处死大鼠,断头取脑,梗死边缘半暗带组织行Western blot和荧光定量PCR(RT-PCR)检测PPARγ表达水平,比色法检测髓过氧化物酶(myeloperoxidase,MPO)活性。结果FNS组能改善神经功能评分,PPARγ表达水平随溶栓再灌注时间呈逐渐增高的趋势,表达高峰可能在梗死后9 h前后,Western blot和RT-PCR检测结果均提示3、6、9、15 h FNS组与其对照组比较差异有统计学意义(P<0.05);6、12 h和15 h FNS组脑梗死边缘区MPO活性与对照组比较差异有统计学意义(P<0.05)。结论 FNS对脑梗死大鼠有保护作用,并可适当延长大鼠局灶脑缺血溶栓时间窗,该作用可能与PPARγ介导的炎性调控作用有关。
Objective To investigate the effect of pre-electrical stimulation of fastigial nucleus stimulation (FNS) on the time window of focal cerebral ischemia and thrombolysis in rats with central nervous system endogenous neuroprotection, and to explore the mechanism of PPARγ- Suppression of the role of prognosis. Methods Sixty Sprague-Dawley rats were randomly divided into FNS group and control group according to random number table method, with 30 rats in each group. FNS group was given electrical stimulation of cerebellar apical nucleus for 1 h, immediately after the completion of electrical stimulation rat middle cerebral artery occlusion (MCAO) model was prepared; control group was not electrical stimulation of cerebellar fastigial nucleus, only MCAO model. Thrombolysis was performed at 1, 3, 6, 9, 12 and 15 h after embolization, respectively. Neurological function was assessed at 72 h after thrombolysis. Rats were sacrificed, The expression of PPARγ was detected by PCR (RT-PCR), and myeloperoxidase (MPO) activity was detected by colorimetric assay. Results The FNS group could improve the score of neurological function and the expression level of PPARγ gradually increased with the time of thrombolytic reperfusion. The expression peak may be around 9 h after infarction. The results of Western blot and RT-PCR showed that 3, 6, 9, There was significant difference between the 15 h FNS group and the control group (P <0.05). The MPO activity in the FNS group at 6, 12 and 15 h after cerebral infarction had significant difference compared with the control group (P <0.05). Conclusion FNS has a protective effect on cerebral infarction in rats and can prolong the time window of focal cerebral ischemia and thrombolysis in rats. This effect may be related to the inflammatory regulation mediated by PPARγ.