Abstract
Objective To investigate the effects of electroacupuncture (EA) at Quchi (LI11) and Zusanli (ST36) on the regulations of neuronal mitochondrial apoptosis pathway in rats with cerebral ischemia-reperfusion (IR) injury.Methods Sixty male adult Sprague-Dawley rats were randomly and evenly divided into three groups:a sham control group (SC),an ischemia control group (IC),and an electroacupuncture group (EA),with 20 rats in each group.After 2 h of ischemia caused by middle cerebral artery occlusion (MCAO) followed by 3 d of reperfusion,IR model was established in IC group and EA group.Finally,there were 18 successful model rats in IC and EA groups,respectively.Rats in EA group received EA at Quchi and Zusanli acupoints beginning at 24 h after MCAO.Neurological deficit induced by IR injury were assessed by using Zea Longa method.The infarct volume was determined at 3 days after IR injury using TTC staining.Apoptotic cells in the cerebral cortex were quantified under confocal fluorescence microscope using TUNEL staining.The expressions of Bcl-2 and Bax were assessed by Western blotting and RT-PCR.Cleaved caspase-3-positive cells at ischemic penumbra of cerebral cortex were detected through immunohistoehemistry method.Results Comparison in the group showed that at the time of 3 d postoperation neurological deficit scores ofIC group (1.67±0.58) and EA group (1.14±0.37) were lower than at the time of 2 h,1 d and 2 d postoperation(P ＜ 0.05).EA group scored significantly lower than IC group in terms of neurological deficit at the time of 2 d and 3 d postoperation(P ＜ 0.05).At 3 d postoperation,infarct volume of EA group reduced significantly(P ＜ 0.05).In SC,IC and EA group apoptotic nerve cells percentage were (1.07 ± 0.02) ％,(39.4 ±10.1)％,(15.1 ±4.2)％,respectively.Compared with IC group,the number of apoptotic nerve cells reduced greatly in EA group(P ＜ 0.05).The expressions of Bcl-2 at the protein and mRNA levels in IC and EA groups were lower than SC group(P ＜ 0.05),however those in EA group were higher than those in IC group(P ＜ 0.05).On the contrary,the expressions of Bax at protein and mRNA levels in IC and EA groups were higher than that in SC group (P ＜ 0.05).Compared with IC group the Bax expression was inhibited in EA group(P ＜ 0.05).Moreover,the number of cleaved caspase-3-positive cells in EA group decreased significantly compared with IC group (P ＜ 0.05).Conclusions EA treatment at acupoints of Zusanli (ST36) and Quchi (LI1 1) exerted the neuroprotective effect on the cerebral IR injury through the modulation of related factor of mitochondrial apoptosis pathway. Key words: Electroacupuncture; Cerebral ischemia-reperfusion; Neuroprotection; Mitochondrial apoptosis
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