Xiao Yao, Hafeez Adam, Zhang Ying, Liu Shimeng, Kong Qingtao, Duan Yunxia, Luo Yumin, Ding Yuchuan, Shi Huaizhang, Ji Xunming
Neurol Res. 2015 May;37(5):447-53. doi: 10.1179/1743132815Y.0000000032. Epub 2015 Mar 28.
Local electrical stimulation (ES) was reported to protect the brain during ischaemic injury, while the protective effect of limb remote ischaemic postconditioning (RIPostC) was confirmed. The aim of this study was to explore whether remote peripheral nerve ES exerted neuroprotection and whether this procedure shared the same neuroprotective mechanism underlying RIPostC.
Stroke in Sprague-Dawley rats was induced by distal middle cerebral artery occlusion (dMCAO). Rats were divided into five groups: dMCAO, RIPostC, ES, nerve resection (NR) + ES and RIPostC+ES. Twenty-four hours after reperfusion, rats were examined for neurobehavioural function, including forelimb fault placing test, Ludmila Belayev 12 score test, and infarct volume. The expression of Bcl-2 and cleaved-caspase-3 in ischaemic cortex was assessed by Western blot.
In forelimb fault placing test, as compared to the highest score in the stroke-only group, RIPostC, ES and RIPostC+ES groups showed a significantly (P < 0.01) lower score. The results were similar for the Ludmila Belayev 12 score test. The infarct volume of the treatment groups also exhibited significant (P < 0.01) reduction as compared to the stroke-only group. The volume of infarct tissue in the combination of RIPostC+ES was significantly less than RIPostC and ES alone (P < 0.05). Furthermore, NR blocked the ES's protection (P < 0.05) as compared to the ES group by using above-mentioned methods. Bcl-2 was upregulated, while cleaved-caspase-3 was downregulated in the experimental groups as compared to the control group. No difference was found among the experimental groups.
Peripheral nerve ES appears to have a neuroprotective effect in a rat dMCAO model. This effect may indicate a neural protective mechanism underlying beneficial effect of RIPostC.
据报道,局部电刺激(ES)可在缺血性脑损伤期间保护大脑,同时肢体远程缺血后适应(RIPostC)的保护作用也得到了证实。本研究的目的是探讨远程外周神经ES是否具有神经保护作用,以及该过程是否与RIPostC具有相同的神经保护机制。
通过大脑中动脉远端闭塞(dMCAO)诱导Sprague-Dawley大鼠发生中风。将大鼠分为五组:dMCAO组、RIPostC组、ES组、神经切除术(NR)+ES组和RIPostC+ES组。再灌注24小时后,对大鼠进行神经行为功能检查,包括前肢错误放置试验、Ludmila Belayev 12分试验和梗死体积。通过蛋白质免疫印迹法评估缺血皮层中Bcl-2和裂解型半胱天冬酶-3的表达。
在前肢错误放置试验中,与单纯中风组的最高分相比,RIPostC组、ES组和RIPostC+ES组的得分显著降低(P<0.01)。Ludmila Belayev 12分试验的结果相似。与单纯中风组相比,治疗组的梗死体积也显著减小(P<0.01)。RIPostC+ES联合组的梗死组织体积明显小于单独的RIPostC组和ES组(P<0.05)。此外,与ES组相比,采用上述方法时,NR阻断了ES的保护作用(P<0.05)。与对照组相比,实验组中Bcl-2上调,而裂解型半胱天冬酶-3下调。实验组之间未发现差异。
外周神经ES在大鼠dMCAO模型中似乎具有神经保护作用。这种作用可能表明RIPostC有益作用的潜在神经保护机制。