黄芪总苷对大鼠局灶性脑缺血/再灌注损伤后BDNF、TrkB和p75NTR mRNA表达的影响

目的观察黄芪总苷(astragalosides,AST)对大鼠局灶性脑缺血/再灌注损伤后的神经保护作用,并探讨其作用机制。方法采用大脑中动脉线栓法制备大鼠局灶性脑缺血(MCAO)再灌注模型,观察AST对大鼠缺血/再灌注损伤后1、3、7和14 d的神经功能的影响;采用RT-PCR方法,观察AST对脑组织BDNF和p75NTR mRNA表达的影响;采用Real-time PCR方法,观察AST对脑组织TrkB mRNA表达的影响。结果AST(40 mg.kg-1)在ig后3 d可以明显降低模型大鼠神经功能评分;在3、7和14 d可以提高脑组织中BDNF mRNA的表达;在7 d和14 d可以降低脑组织中p75NTR mRNA的表达,提高TrkB mRNA表达。结论AST对大鼠局灶性脑缺血/再灌注损伤后的神经功能恢复有一定的促进作用,其机制可能与促进BDNF和TrkB mRNA表达、抑制p75NTR mRNA的表达有关。

Effects of astragalosides on the expression of BDNF, TrkB and p75NTRmRNA against focal cerebral ischemia-reperfusion injury

Aim To observe the neurological protective effects of astragalosides(AST) on focal cerebral ischemia-reperfusion(I/R) injury in rats and to explore its possible mechanism.Methods Male SD rats received right middle cerebral artery occlusion for 120 min,and were decapitated 1,3,7,and 14 days after reperfusion.AST(40 mg·kg-1) was orally administered after I/R.Neurological deficit score was daily determined,the expressions of BDNF and p75NTR mRNA were detected by RT-PCR,and the expression of TrkB mRNA was detected by real-time PCR.Results AST reduced the neurological deficit score on days 3,increased the expression of BDNF mRNA on days 3,7 and 14,decreased p75NTR mRNA and increased TrkB mRNA on days 3 and 7.Conclusions AST improves the neurological deficits after I/R in rats.The mechanism may be related with increasing BDNF,and TrkB mRNA,and decreasing p75NTR mRNA.