【摘要】 目的探讨电针对缺血性脑损伤后突触可塑性促进作用的机制。方法采用热凝闭大鼠大脑中动脉致局灶性脑缺血模型(MCAO),研究缺血2周(2w)和5周(5w)后缺血区皮层突触超微结构、突触素P38、神经生长相关蛋白43(GAP43)、脑源性神经营养因子(BDNF)、神经生长因子(NGF)的变化规律和电针对其影响。结果两个缺血组缺血脑区皮层突触的面数密度(Nv)、突触连接带面密度(Sv)、突触的体密度(Vv)和突触后致密物质(PSD)、缺血脑区皮层突触素P38的表达均较假手术组同期明显减少和下降(P<0.01)。在缺血组和治疗组中,5w组的Nv和Sv均多于2w组(P<0.01);两个治疗组缺血区皮层Sv均较同时段的缺血组显著上升(P<0.01),而PSD在治疗5w时明显高于缺血5w组和治疗2w组(P<0.01),电针对Vv和突触界面曲率影响较小。缺血5w组与缺血2w组比较,突触素P38表达明显升高(P<0.01),治疗2w组与缺血2w组比较,差异无显著性(P>0.05),治疗5w组与缺血5w组比较明显增加(P<0.01)。缺血2w组和治疗2w组缺血区周围皮层GAP43表达与假手术组比较,均显著增加(P<0.01),但两组比较差异无显著性(P>0.05)。缺血5w组与假手术组比较差异无显著性(P>0.05),治疗5w组与假手术5w组比较明显增加(P<0.01)。两个缺血组缺血脑区周围皮层NGF、BDNF的免疫阳性细胞数量较假手术组明显增多(P<0.01),治疗组免疫阳性细胞的表达与同时段缺血组比较,显著增高(P<0.01),缺血组和治疗组随时间的推移表达均呈下降趋势(P<0.01)。结论提示电针可能通过保护与改善MCAO模型大鼠缺血脑区皮质的突触超微结构,提高突触素P38、GAP43、NGF和BDNF的表达,促进脑缺血后突触可塑性的形成。更多还原

【Abstract】 ObjectiveTo explore the mechanisms of electro-acupuncture (EA) in improving synaptic plasticity after cerebral ischemic injury. MethodsFocal cerebral ischemia (FCI) model was established by middle cerebral artery occlusion (MCAO) with heat-coagulation method. The changing rules of synaptic ultrastructure, synaptophysin (P38), growth-associated protein-43 (GAP-43), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the ischemic cortex 2 and 5 weeks after FCI and the effects of EA on them were observed. ResultsExpression of numerical density (Nv), surface density (Sv), volume density (Vv), post synaptic density (PSD) and P38 in the ischemic cortex significantly decreased after MCAO (P<0.01). Among them, Nv and Sv were raised at the 5th week in FCI rats either treated or untreated with EA (P<0.01), but the increment of Sv was higher in those of the treated rats (P<0.01); PSD in the EA treated rats also showed a significant increase at the 5th week, which was significant higher than that in those untreated; EA showed insignificant influence on Vv and synaptic interfacial curvature; P38 lowered continuously after 2 weeks, but at the 5th week, it was higher in EA treated rats than that in untreated rats (P<0.01), while at the 2nd week, the levels in treated and untreated rats were equal. GAP-43 rose in the 2nd week after modeling, with no difference between EA treated and untreated animals, at the 5th week, it was lowered in untreated rats to near that in sham-operated rats, but maintained at higher level in EA treated rats; NGF and BDNF positive cells significantly increased after modeling (P<0.01), and showed a descending trend with the time going (P<0.01) both in rats treated or untreated with EA. ConclusionEA can protect synaptic ultrastructure, promote the expression of P38, GAP-43, NGF and BDNF in the ischemic cerebral cortex, and thus improve synaptic plasticity in cerebral ischemic rats.更多还原