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目的探讨运动干预对慢性应激模型大鼠抑郁行为及不同脑区细胞外信号调节蛋白激酶(ERK)-环磷酸腺苷反应元件结合蛋白(CREB)信号通路磷酸化水平变化。方法 40只雄性SD大鼠随机分为对照组、应激组、运动组、运动+应激组,采用慢性温和不可预知性应激方法建立抑郁症模型;采用旷场实验及糖水消耗实验进行行为学测定,免疫组织化学方法检测海马、额叶皮层磷酸化ERK(p-ERK)及磷酸化CREB(p-CREB)表达变化。结果与对照组比较,慢性应激大鼠水平运动评分[(20.4±11.67)分]、垂直运动评分[(5.4±2.36)分]、体重增加量[(29.82±17.68)g]和糖水摄入量[(8.13±2.56)g]均减少(P<0.01),海马、额叶皮层p-ERK[(6.15±2.86)、(12.43±5.14)]及p-CREB[(2.89±0.51)、(2.34±0.53)]表达均降低(P<0.01);与应激组比较,运动+应激组大鼠水平运动评分[(48.2±22.66)分]、垂直运动评分[(13.1±3.06)分]、体重增加量[(76.50±25.81)g]和糖水摄入量[(17.02±4.13)g]均升高;与对照组比较,运动组各脑区P-ERK/P-CREB[(23.76±4.11)、(32.64±5.37)、(6.73±0.55)、(5.79±0.51)]磷酸化水平均升高(P<0.05)。结论运动具有一定抗抑郁样行为学效应,其分子机制可能与上调脑内ERK/CREB信号通路的磷酸化水平有关。
Objective To investigate the effects of exercise on the depression and the phosphorylation of extracellular signal-regulated kinase (ERK) -catenin (CREB) signaling pathway in chronic stress rats. Methods Forty male Sprague-Dawley rats were randomly divided into control group, stress group, exercise group and exercise + stress group. Chronic mild unpredictable stress model was used to establish depression model. Open-field and sugar consumption experiments The expressions of phosphorylated ERK (p-ERK) and phosphorylated CREB (p-CREB) in the hippocampus and frontal cortex were detected by immunohistochemistry. Results Compared with the control group, the level of exercise in chronic stress rats [(20.4 ± 11.67) points], the score of vertical movement (5.4 ± 2.36), the weight gain [(29.82 ± 17.68) g] The levels of p-ERK in hippocampus and frontal cortex [(6.15 ± 2.86), (12.43 ± 5.14)] and p-CREB [(2.89 ± 0.51), (P <0.01). Compared with the stress group, the level of exercise in the exercise + stress group was significantly higher than that in the stress group [(48.2 ± 22.66) vs [13.1 ± 3.06] (P <0.05). Compared with the control group, P-ERK / P-CREB [(23.76 ± 4.11), (32.64 ± 5.37), (6.73 ± 0.55) and (5.79 ± 0.51)], respectively (P <0.05). Conclusions Exercise has certain antidepressant-like behavioral effects, and its molecular mechanism may be related to the up-regulation of phosphorylation of ERK / CREB signal pathway in the brain.