摘要
目的:探讨电针对血管性痴呆(VD)大鼠学习记忆障碍的治疗效应及其作用的分子机制。方法:200—220g雄性大鼠60只,除假手术组10只外,其他均用4-VO法造模后,存活大鼠随机分为:电针组14只,尼莫通组13只,模型组13只。电针组针刺“百会”和“大椎”两穴,尼莫通组以剂量12mg/kg给药,假手术组与模型组未予任何治疗。治疗20天后.采用Morris水迷宫评价大鼠学习记忆能力变化,采用免疫组化法观察Bcl-2和Bax的蛋白表达变化,采用RT—PCR法观察HO—1mRNA表达变化。结果:与模型组比较,电针组逃避潜伏期、皮质和海马Bax蛋白表达显著减少(P〈0.01),HO~1总mRNA吸光度比值显著降低(P〈0.05),Bd-2蛋白表达显著增加(P〈0.01)。结论:电针治疗能够改善VD模型大鼠学习记忆能力,能够减少皮质海马神经细胞Bax和HO-1蛋白表达,增加Bd-2蛋白表达。
Objective: Through researches we can know the effect and molecule mechanism on VD by EA comprehensively, Methods: 4 - VO method was used to establish the models of the global ischemia and reperfusion in 60 SD male rats and animals were divided into sham - operated control group, VD model group, EA group and Nimotop therapeutic group. The animals of EA groups were stimulated at the point of Baihui and Dazhui by EA, Nimotop therapeutic group were given Nimotop 12mg/kg once a day. There was no other treating ways in sham - operated and VD model group. After treatments we adopted Morris water maze to test behavior of memory and study, adopted immunohistochemical method to test bcl -2 and Bax, adopted RT -PCR technique to test gene expression of HO - 1. Result :In place test, eomparing to VD model group,the escape latent period and Bax protein expression of EA group and Nimotop therapeutic group decreased obviously( P 〈0.01 ) ,the ratio of HO - 1 mRNA absorbency decreased obviously( P 〈 0.05 ), Bcl - 2 protein expression increased obviously ( P 〈 0. 0 1 ). Conclusions :EA therapy can improve the learning and memory ability of VD model rats, and decrease Bax and HO - 1 protein expression in neuron orotortical area and hippocampal commissure ,increase Bcl- 2 protein expression.
出处
《辽宁中医杂志》
CAS
北大核心
2006年第11期1510-1512,共3页
Liaoning Journal of Traditional Chinese Medicine