摘要
目的:探讨海马神经发生在电针治疗癫痫大鼠中的作用机制。方法:选用氯化锂-匹罗卡品制备癫痫大鼠模型,观察电针治疗1周、3周和4周后自发性反复癫痫发作(SRS)的次数,同时采用免疫组织化学方法观察5-溴脱氧嘧啶尿核苷(BrdU)标记的海马齿状回新生神经元增殖的数量。结果:癫痫持续状态后存活下来的大鼠最早在致痫后3天即出现SRS,第2周起模型组和电针组均呈现SRS。治疗3周和4周后,电针组SRS的次数均较模型组明显减少(P<0.05)。模型组大鼠致痫后第1周和第3周,BrdU免疫阳性细胞数目较空白组显著增加(P<0.01),至第4周明显减少,与空白组相当。电针组治疗第1周,BrdU免疫阳性细胞数目虽然较模型组减少,但差异无显著性意义(P>0.05);治疗第3周,BrdU免疫阳性细胞数目较模型组明显减少(P<0.05),第4周细胞数目与模型组、空白组相当。结论:电针能显著抑制癫痫大鼠海马齿状回的神经发生,可能在电针治疗癫痫中发挥重要作用。
Objective: To observe the possible effect of hippocampal neurogenesis on electroacupuncture (EA) in treating epilepsy rats. Methods: Epilepsy rats models were induced with lithium chloride-pilocarpine. The frequency of spontaneous recurrent seizures (SRS) was observed after EA for 1,3 and 4 week(s). Immunohistochemical assay was used to detect the number of neoformative neurons with 5-bromo-2-deoxyuridine (Brdu) positive in hippocampal dentate gyrus. Results: Earliest SRS occurred in the survival rats at epileptic state 3 days after the onset of epilepsy. From the second week,SRS was found in the model group and EA group. After EA for 3 and 4 weeks,the frequency of SRS was reduced in EA group ( P < 0. 05 compared with the model group).The number of Brdu-positive neurons was increased in the model group one week and 3 weeks after the onset of epilepsy( P < 0. 01 compared with the blank group),and decreased to the level of blank group from the fourth week. On the first week of EA,the number of Brdu-positive neurons was decreased,but the difference was insignificant as compared with the model group ( P > 0. 05 ),and then the decrease was obvious on the third week ( P < 0. 05).The number of Brdu-positive neurons in EA group arrived to the level in the model group and blank group on the fourth week of EA. Conclusion: EA can inhibit the hippocampal neurogenesis in the hippocampal dentate gyrus of epilepsy rats,indicating that hippocampal neurogenesis plays an important role in the therapeutic effect of EA.
出处
《新中医》
CAS
北大核心
2010年第8期117-119,共3页
New Chinese Medicine
基金
广东省自然科学基金(编号:07004846)
