电针对慢性应激抑郁模型大鼠海马神经干细胞巢蛋白的影响

目的 观察电针对慢性应激抑郁模型大鼠海马神经干细胞巢蛋白（Nestin）的影响.方法 将雄性SD大鼠按照数字表法随机分为健康组、模型组、电针组和氟西汀组,每组10只.采用慢性不可预知温和应激结合孤养的方法制备模型.电针组选取＂印堂穴＂和＂百会穴＂,接HANS LH202H型电针仪,频率2 Hz,电流强度0.6 mA,治疗30 min,每天1次,共21 d.氟西汀组大鼠按3.3 mg/kg腹腔注射氟西汀,每天1次,共治疗21 d.用游泳不动时间测行为学,用免疫组化检测海马神经干细胞Nestin的表达.结果 健康组、模型组、电针组、氟西汀组大鼠游泳不动时间分别为（14.40±2.17）s、（37.50±7.69）s、（30.10±4.53）s、（32.10±4.98）s.与健康组比较,模型组大鼠游泳不动时间显著延长（t=7.53,P＜0.01）,海马神经干细胞Nestin阳性表达降低（P＜0.01）.与模型组比较,电针组、氟西汀组大鼠游泳不动时间明显减少（F=4.89,P＜0.05）,海马神经干细胞Nestin阳性表达增强（χ^2=12.057,P＜0.01）,电针组与氟西汀组之间差异无统计学意义（χ^2=3.899,P＞0.05）.结论 应激引起大鼠海马神经干细胞巢蛋白表达降低,而电针刺激可以促进抑郁模型大鼠海马神经干细胞增殖,改善慢性应激大鼠的行为表现.这可能是电针对慢性应激抑郁模型大鼠海马损伤的保护作用机制之一.

Influence of electroacupuncture on nestin expression in hippocampus neural stem cells of the chronic stress induced depression model rats

Objective To investigate the effect of electroacupuncture （EA） on changes of nestin expression in hippocampus neural stem cells of chronic stress model rats. Methods According to the random number table ,40 male SD rats were evenly randomized into the normal, stress-model, fluoxetine and EA groups. Chronic stress model rats were subjected to successive 21 days of seven different ways of chronic stress ,while received EA and fluoxetine as treatment method. EA（2 Hz,0.6 mA,30 rain） was applied to ＂ Baihui＂ （ GV 20） and ＂ Yintang＂ （ EX-HN 3 ）, once daily,continuously for 21 days. Fluoxetine（3.3mg/kg） was given by intraperitoneal injection,once daily. The rats＇behavior was observed by calculating immobility time in forced swimming test. The nestin expression in hippocampus neural stern cells was detected by immunohistochemical method. Results The immobility time in the forced swimming test of control group, model group, EA group, fluoxetine group were （ 14.40 ± 2.17 ） s, （ 37.50 ± 7.69 ） s, （ 30.10 ± 4. 53 ）s and （32.10 ± 4.98 ）s, respectively. Compared with the control group, the immobility time in forced swimming test prolonged significantly in the model group（ t = 7.53 ,P 〈 0.01 ）, and the expression of nestin in hippocampus neu- ral stem cells decreased in the model group （P 〈 0.01 ）. In comparison with the model group, the immobility time in forced swimming test shortened significantly in both EA and fluoxetine group （ F = 4.89, P 〈 0.05 ） , and the expression of nestin in hippocampus neural stem cells increased in both EA and fluoxetine group （ X2 = 12. 057, P 〈 0.01 ）. No significant difference was found between the EA group and the fluoxetine group （ X2 = 3. 899, P 〉 0. 05 ）. Condus｜on Chronic stress may cause the model rats to move less ,whereas EA could promote recovery of the rats＇abnormal behavior, and stimulate proliferation of hippocampus neural stem cells,which may be one of the mechanism of the protective effect of EA on hippocampus injury in chronic stress model rats.