星状神经节阻滞抑制脑缺血再灌注大鼠神经元变性、神经炎症与NF-κB信号活性

Stellate ganglion block inhibits neurological dysfunction,neuronal degeneration,neuroinflammation and NF-κB signaling activity in cerebral ischemia-reperfusion rats

目的探讨星状神经节阻滞(stellate ganglion block,SGB)对脑缺血/再灌注(ischemia/reperfusion,I/R)大鼠神经功能恢复的影响及机制。方法通过改良尼龙线栓法建立大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)模型来模拟脑缺血/再灌注损伤,并在MCAO术后1 d对大鼠进行SGB术干预。MCAO术后7 d,通过mNSS评分、转棒实验和跑梯实验评估大鼠的神经功能;通过Nissl、Fluro-Jade B和NeuN染色评估海马CA1区神经元形态;通过IBA-1染色评估海马CA1区中小胶质细胞活化情况;通过ELISA法检测海马CA1区中TNF-α、IL-1β和IL-10的水平;通过Western blot检测NF-κB通路相关蛋白表达水平。结果脑I/R大鼠mNSS评分、总失步数和转棒停留时间均明显增加,海马CA1区中神经元明显丢失和变性、IBA-1免疫反应性明显增强,TNF-α和IL-1β水平明显增加,抑炎因子IL-10水平明显降低;SGB对脑I/R的上述效应具有明显抑制作用。结论SGB能改善脑I/R后大鼠的神经功能,这一作用可能与其抑制海马CA1区脑组织中NF-κB信号通路活性并降低神经炎症和神经元变性有关。

Objective To investigate the effect and the mechanism of stellate ganglion block(SGB)on neurological function recovery in cerebral ischemia/reperfusion(I/R)rats.Methods Middle cerebral artery occlusion(MCAO)model was established to simulate the cerebral I/R injury by using modified sucrose occlusion method,and SGB was performed at 1 d after MCAO.At 7 days after MCAO,the neurological function of rats was evaluated by mNSS score,rotarod test and run staircase test;the pathological morphology of hippocampal CA1 neurons was evaluated by Nissl,Fluro-Jade B and NeuN staining;activation of microglial cells in hippocampal CA1 region was assessed by IBA-1 staining;the levels of TNF-α,IL-1βand IL-10 in hippocampal CA1 region were detected by ELISA;the expression levels of NF-κB pathway related proteins were detected by Western blot.Results mNSS score,total step loss and retention time of stick rotation were significantly increased in cerebral I/R rats,and the loss and degeneration of neurons in hippocampal CA1 region was significantly enhanced,the immunoreactivity of IBA-1 was significantly increased,the levels of TNF-αand IL-1βwere significantly increased,while IL-10 level was significantly decreased.SGB significantly inhibited the above effects of cerebral I/R.Conclusion SGB can improve the neural function of rats after cerebral I/R,which may be related to the inhibition of NF-κB signaling pathway activity in hippocampal CA1 region and the decrease of neuroinflammation and neuronal degeneration.