Lin Ruhui, Xia Jinyan, Ma Xiaohan, Li Zuanfang
Innovation and Transformation Center, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2024 Dec 20;44(12):2317-2326. doi: 10.12122/j.issn.1673-4254.2024.12.07.
To explore the neuroprotective mechanism of electroacupuncture at the acupoints and in rats with cerebral ischemia-reperfusion (IR) injury.
Forty-eight male SD rats were equally randomized into sham operation group, cerebral IR model group, acupoint electroacupuncture group and non-acupoint acupuncture group. In the latter 3 groups, cerebral focal ischemic injury was induced using the Longa method; in the two electroacupuncture groups, electroacupuncture was performed either at the acupoints and or at non-acupoint sites for 7 days. The changes in neurological deficit scores, cerebral infarction volume, learning and memory function, pathologies in hippocampal CA1 area, neuronal and synaptic ultrastructures, and synaptic density of the rats were observed, and serum GABA level and mRNA and protein expressions of GABAR α1, CaMK II, SYN1 and PSD-95 in the hippocampal tissue were detected.
Compared with those in cerebral IR model group, the rats receiving electroacupuncture at the acupoints, but not those with electroacupuncture at the non-acupoints, showed significantly decreased neurological deficit scores and cerebral infarction volume with shortened escape latency and increased platform crossings. Electroacupuncture at the acupoints significantly increased neuronal cell number, decreased the width of the synaptic gaps and increased density of synaptic bodies in the ischemic hippocampal CA1 area, resulting also in increased serum GABA levels and hippocampal expressions of GABARα1, SYN1 and PSD-95 and lowered expression level of CaMK II.
Electroacupuncture at and improves learning and memory function of rats with cerebral IR injury possibly through a mechanism that promotes synaptic regeneration, upregulates hippocampal expressions of GABAAR α 1, SYN1 and PSD-95 and downregulates the expression of CaMK II.
探讨电针穴位对脑缺血再灌注(IR)损伤大鼠的神经保护机制。
将48只雄性SD大鼠随机分为假手术组、脑IR模型组、穴位电针组和非穴位针刺组。后3组采用Longa法诱导脑局灶性缺血损伤;在两个电针组中,分别在穴位或非穴位进行电针治疗7天。观察大鼠神经功能缺损评分、脑梗死体积、学习记忆功能、海马CA1区病理学、神经元和突触超微结构以及突触密度的变化,并检测血清GABA水平以及海马组织中GABARα1、CaMK II、SYN1和PSD-95的mRNA和蛋白表达。
与脑IR模型组相比,穴位电针组大鼠神经功能缺损评分和脑梗死体积显著降低,逃避潜伏期缩短,平台穿越次数增加,而非穴位电针组大鼠无此变化。穴位电针显著增加了缺血海马CA1区神经元细胞数量,减小了突触间隙宽度,增加了突触体密度,还导致血清GABA水平升高以及海马组织中GABARα1、SYN1和PSD-95表达增加,CaMK II表达水平降低。
电针穴位可能通过促进突触再生、上调海马组织中GABAARα1、SYN1和PSD-95的表达以及下调CaMK II的表达来改善脑IR损伤大鼠的学习记忆功能。