推拿对慢性应激大鼠抑郁行为的影响及其机制

目的: 探讨推拿对慢性应激大鼠抑郁行为的影响及其作用机制。方法: 制备慢性轻度不可预见性的应激大鼠模型^1-2],造模21 d后,进行推拿治疗14 d。分组:空白对照组、模型组、推拿组、氟西汀组,每组10只。每日推拿膀胱经重要穴位10 min(间隔2 min,共2次)。通过体质量检测、旷场、糖水消耗实验和水迷宫实验评价抑郁模型大鼠行为学改变情况;蛋白质免疫印迹法(Western blot)法检测大鼠海马及前额叶皮质组织中ERK/P-ERK、BDNF蛋白表达情况。结果: 模型组与空白组比较,大鼠的体质量、旷场、糖水消耗实验和水迷宫数据均显著下降(P＜0.01),P-ERK、BDNF蛋白含量均显著降低(P＜0.01);推拿组和氟西汀组与模型组比较,大鼠的体质量、旷场实验、糖水消耗实验和水迷宫实验数据均显著上升(P＜0.01),推拿组和氟西汀组大鼠海马及前额叶皮质组织中P-ERK、BDNF蛋白含量均显著升高(P＜0.05,P＜0.01),氟西汀组升高更为显著(P＜0.01)。结论: 推拿可上调大鼠海马及前额叶皮质组织中ERK蛋白的磷酸化水平,激活ERK信号通路,促进效应蛋白BDNF的表达,改善慢性应激大鼠的抑郁行为。

Effect of massage on depressive behavior of chronic stress rats and its mechanism

Objective: To investigate the effects and mechanisms of massage on the depressive behavior of rats with chronic stress. Methods: The rats were subjected to chronic unpredictable mild stress for 21 days and then treated with massage for 14 days. They were divided into the following groups: blank control group, model group, massage group and fluoxetine group, with 10 rats in each group. The important acupoints of bladder meridian were massaged for 10 minutes every day (with an interval of 2 minutes, 2 times in total). Body weight, open field test, sucrose intake test and water maze test were used to evaluate the behavioral changes. The expressions of Erk/p-ERK (Extracellular signal-related kinases/Phosphorylation extracellular signal-related kinases) and BDNF in prefrontal cortex were detected by Western Blot. Results: The body weight, open field sucrose intake test and water maze data of the model group were significantly lower than those of the Control Group (P＜0.01), and the contents of p-ERK and BDNF protein in prefrontal cortex were decreased significantly (P＜0.01). The body weight, open field test, sucrose intake test and water maze test data of rats in massage group and fluoxetine group were significantly higher than those in model group(P＜0.01). The contents of p-ERK and BDNF in frontal cortex were increased significantly (P＜0.05, P＜0.01), especially in fluoxetine group (P＜0.01). Conclusion: Massage may increase the phosphorylation level of ERK protein in hippocampus and prefrontal cortex, activate ERK signaling pathway, promote the expression of BDNF, and improve the depression behavior of chronic stress rats.