摘要
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。
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 rain, and were decapitated 1, 3, 7, and 14 days after reperfusion. AST （40mg·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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2009年第5期672-676,共5页
Chinese Pharmacological Bulletin
基金
安徽省自然科学基金资助项目(No00144414)
安徽省教育厅自然科学基金资助项目(NoKJ2008B301)
安徽省高校自然科学研究项目(NoKJ2009A81)
安徽省高等学校青年教师科研资助项目(No2008jq1059zd)
