摘要
目的观察大鼠局灶性脑缺血后脑源性神经营养因子和神经生长抑制因子Semaphorin 3A(Sema 3A)的表达,探讨脑缺血损伤与脑源性神经营养因子、Sema 3A的关系及葛根素对脑缺血损伤的保护作用。方法建立Wistar大鼠永久大脑中动脉闭塞模型,应用免疫组织化学法观察不同缺血时间脑源性神经营养因子和Sema 3A阳性神经元数的动态改变。结果脑源性神经营养因子阳性神经元自缺血6 h开始增多,1天达高峰,治疗组阳性神经元较缺血组增多(P<0.05)。Sema 3A阳性神经元自缺血6 h开始增多,1天达高峰,3天达正常对照组水平,治疗组阳性神经元较缺血组减少(P<0.05)。结论脑缺血后脑源性神经营养因子和Sema 3A的表达均有短暂上调,可能与神经元的损伤修复再生机制有关。葛根素治疗后脑源性神经营养因子的表达增加,Sema 3A的表达下降,提示葛根素对脑缺血损伤具有保护作用。
Aim To observe the expression of braln-derived neurotrophic factor (BDNF) and Semaphorin 3A (Sema 3A) after focal cerebral ischemia , and to study the neuroprotective effects of puerarin. Methods The medd of focal cerebral ischemia was established by occluding middle cerebral artery (MCAO). Dynamic changes of BDNF and Sema 3A positive neurons at different time were observed with method of immunohistochemistry. Results The number of BDNF positive neurons inerased after 6 h of ischemia, and reached its peak at the time of 1 d after ischemia. Compared with treatment group and ischemic group, the levels of BDNF were higher ( P 〈 0.05) ; the number of Sema 3A positive neurons increased after 6 h of ischemia, and reached its peak at the time of 1 d after ischemia, then become normal after 3 d. Compared with treatment group and ischemic group,the levels of Sema 3A were lower ( P 〈 0.05). Conclusions After the attack of cerebral ischemia, the expression of BDNF and Sema 3A may he related to the mechanism of neuronic injury and repairment. Puerarin may have protective effects on ischemic neurons.
出处
《中国动脉硬化杂志》
CAS
CSCD
2006年第10期872-874,共3页
Chinese Journal of Arteriosclerosis