健脾补土方对脑缺血/再灌注损伤大鼠NF-κB和IκBα蛋白表达水平的影响

Effects of Jianpi Butu Prescription on the Expression of NF-κB and IκBα in Rats with Cerebral Ischemia/Reperfusion Injury

目的通过观察健脾补土方对脑缺血/再灌注(I/R)损伤大鼠脑组织核因子-κB(NF-κB)和NF-κB抑制蛋白α(Iκ-Bα)表达的影响,探讨健脾补土方对脑保护作用的部分机制。方法将120只SD大鼠随机分为假手术组,模型组,依达拉奉组,健脾补土方小、中、大剂量组,每组20只。采用线栓法制备大鼠大脑中动脉闭塞再灌注模型,治疗7 d,治疗前后行神经功能缺损评分,应用HE染色观察大脑皮质区细胞的形态学改变;采用Western blot法检测大脑皮质内NF-κB和IκBα蛋白的表达水平。结果与假手术组比较,模型组神经功能缺损评分、NF-κB/p65蛋白的表达显著增加(P<0.01);IκBα蛋白的表达明显减少(P<0.01);与模型组比较,健脾补土方治疗组神经功能缺损评分、NF-κB/p65蛋白的表达均明显减少(P<0.05或P<0.01),IκBα蛋白的表达均明显增加(P<0.05或P<0.01)。结论健脾补土方可能通过抑制脑组织NF-κB的表达,促进IκBα的表达,从而改善I/R损伤大鼠神经功能缺损,对I/R损伤起保护作用。

Objective To explore the mechanism of Jianpi Butu prescription（JPBTP） in cerebral protection by observing the effect of JPBTP on the expression of NF-κB and IκBα in rats with cerebral ischemia /reperfusion（I/R） injury. Methods120 rats were randomly divided into sham-operation group, model group, edaravone group, JPBTP groups（low-dose, middle-dose,and high-dose）, 20 in each group. The models of cerebral I/R injury were induced by middle cerebral artery occlusion, and treated them for 7 days. Neurological severity score was evaluated between before and after treatment, HE staining was used to observe the morphology changes in hippcampus cerebral cortex area. The expression levels of NF-κB and IκBα in cerebral cortex area were detected by Western blot. Results Compared with the sham-operation group, neurological severity score, and the expression level of NF-κB p65 protein in the model group were significantly increased（P〈0.01） and the expression level of IκBα protein was significantly decreased（P〈0.05） in the model group. Compared with the model group, neurological severity score and the expression level of NF-κB/p65 protein were significantly decreased（P〈0.05 or P〈0.01） and the expression level of IκBα protein was significantly increased（P 0.05 or P 0.01） in JPBTP group. Conclusion JPBTP may promote the expression level of IκBα protein in brain tissue by suppressing the expression of NF-κB/p65 protein to improve and protect the neurological deficit of I/R injury rats.