电针预处理对老龄大鼠长期术后认知功能障碍影响及相关机制

Effects of Electroacupuncture Pretreatment on Long-term Postoperative Cognitive Dysfunction and Hippocampal Inflammation in Aged Rats

术后认知功能障碍(postoperative cognitive dysfunction,POCD)是老年人群常见的并发症。一种胆碱能依赖信号,α7-烟碱乙酰胆碱受体(α7-nAChR),已被认为在各种神经系统疾病中调节认知过程。为探讨电针预处理是否能改善老龄大鼠术后长期认知功能障碍以及其可能机制。通过将60只清洁级雄性SD(Sprague-Dawley)大鼠(20月龄)随机分为5组(样本数n=12):假手术组(S组)、模型组(M组)、电针组(EA组)、银环蛇毒+电针组(Y+EA组)、银环蛇毒+模型组(Y+M组)。在术后30 d后,分别对各组采用新物体识别实验评价认知功能,采用尼氏(Nissl)染色检测神经元数量,免疫荧光检测小胶质细胞活化、蛋白质印迹法(Western blot)检测海马IL-6、NF-κB和IL-1β的水平。实验结果表明:电针预处理增加了对新物体的探索,恢复了大鼠术后神经元的数量,降低了小胶质细胞激活,降低海马炎性因子蛋白表达,而α-BGT部分逆转了电针的作用。可见电针预处理改善了老龄大鼠长期术后认知功能障碍和海马炎症,其机制可能与激活α7nAChR介导的胆碱能抗炎通路有关。

Postoperative cognitive dysfunction(POCD)is a common complication in the elderly population.A cholinergic dependent signal,α7-nicotinic acetylcholine receptor(α7-nAChR),has been suggested to regulate cognitive processes in various neurological disorders.To investigate whether electroacupuncture pretreatment can improve long-term postoperative cognitive dysfunction in aged rats and its possible mechanism.Male Sprague-Dawley(SD)rats(20 months old)were randomly assigned to the following 5 groups(number of samples n=12):sham-operated group(S group),model group(M group),electroacupuncture group(EA group),bungatotoxin+electroacupuncture group(Y+EA group),and bungatotoxin+model group(Y+M group).Thirty days post surgery,the novel objective recognition test were used to evaluate cognitive function.Neuronal amount,microglial activation,and levels of NF-κB,interleukin-6(IL-6),and IL-1β,were detected by Nissl staining,immunofluorescence,and Western blot assays.The experimental results show that EA pretreatment increases the exploration of new objects,restores the number of postoperative neurons in rats,reduces the activation of microglia,and decreases the expression of inflammatory factor proteins in the hippocampus,whileα-BGT partially reverses the effect of EA.It can be seen that EA pretreatment improves long-term postoperative cognitive dysfunction and hippocampal inflammation in aged rats,and the mechanism may be related to the activation ofα7nAChR mediated cholinergic antiinflammatory pathway.