电针改善老龄大鼠术后认知功能障碍的机制与海马神经元线粒体途径凋亡的关系

Relationship between mechanism underlying electro-acupuncture-induced improvement of postoperative cognitive dysfunction and mitochondrion-dependent apoptosis in hippocampal neurons of aged rats

目的探讨电针改善老龄大鼠术后认知功能障碍的机制与海马神经元线粒体途径凋亡的关系。方法健康雄性SD大鼠72只,18月龄,体重500~550 g,采用随机数字表法分为3组(n=24):对照组(C组)、手术组(O组)和电针组(EA组)。EA组电针刺激百会和大椎穴30 min,选用疏密波,频率2/15 Hz,强度1 mA,1次/d,连续刺激5 d。电针刺激结束后,O组和EA组在3%七氟醚麻醉下行剖腹探查术。分别于术前1 d、术后3、7 d时行Morris水迷宫实验检测大鼠认知功能,水迷宫实验结束后处死大鼠取海马组织,采用流式细胞术检测神经元凋亡率,采用Western blot法检测caspase-3和细胞色素c(Cyt c)的表达水平。结果与C组比较,O组和EA组术后逃避潜伏期延长,穿越原平台次数减少,海马神经元凋亡率增加,caspase-3和Cyt c表达上调(P<0.05);与O组比较,EA组术后逃避潜伏期缩短,穿越原平台次数增加,海马神经元凋亡率下降,caspase-3和Cyt c表达下调(P<0.05)。结论电针改善老龄大鼠术后认知功能障碍的机制可能与抑制海马神经元线粒体途径凋亡有关。

Objective To evaluate the the relationship between the mechanism underlying electro-acupuncture(EA)-induced improvement of postoperative cognitive dysfunction and mitochondrion-dependent apoptosis in hippocampal neurons of aged rats. Methods Seventy-two healthy male Sprague-Dawley rats, aged 18 months, weighing 500-550 g, were divided into 3 groups(n=24 each)using a random number table method: control group(group C), operation group(group O)and group EA.EA was performed at Baihui and Dazhui acupoints for 30 min using disperse-dense waves, with a frequency 2/15 Hz and intensity 1 mA, once a day for 5 consecutive days in group EA.Laparotomy was performed under 3% sevoflurane anesthesia after the end of EA stimulation in O and EA groups.Morris water maze test was performed on 1 day before operation and 3 and 7 days after operation to assess the cognitive function.Rats were sacrificed after the end of Morris water maze test, brains were removed, and hippocampal tissues were obtained for detection of apoptosis rate of hippocampal neurons and expression of hippocampal caspase-3 and cytochrome c(Cyt c)by Western blot. Results Compared with group C, the escape latency was significantly prolonged after operation, the frequency of crossing the original platform was reduced, the apoptotic rate of hippocampal neurons was increased, and the expression of caspase-3 and Cyt c was up-regulated in O and A groups(P<0.05). Compared with group O, the escape latency was significantly shortened after operation, the frequency of crossing the original platform was increased, the apoptotic rate of hippocampal neurons was decreased, and the expression of caspase-3 and Cyt c was down-regulated in EA group(P<0.05). Conclusion The mechanism by which EA improves postoperative cognitive dysfunction may be related to inhibiting mitochondrion-dependent apoptosis in hippocampal neurons of aged rats.