耐力训练对力竭运动诱导的大鼠淋巴细胞凋亡的影响

Effect of Endurance Training on the Exhaustion-Induced Lymphocyte Apoptosis in Rats

目的 :研究耐力训练对大鼠力竭运动后淋巴细胞凋亡的影响 ,并分析其机制。方法 :将SD大鼠随机分为安静组、力竭运动组、训练 +力竭运动组。训练 +力竭运动组进行 3周游泳耐力训练后 ,除安静组外 ,全部大鼠负重 4 %进行力竭游泳 ,比较运动后即刻大鼠脾细胞、胸腺细胞及外周血液淋巴细胞凋亡率 ,细胞内Ca2 +浓度及血清皮质醇 (C)浓度。结果 :训练 +力竭运动组大鼠力竭游泳时间明显长于力竭运动组 (P <0 . 0 5 ) ;训练 +力竭运动组大鼠外周血淋巴细胞凋亡率较安静组有升高趋势 ,但较力竭运动组有下降趋势 ,脾细胞凋亡率与力竭运动组相近 ,胸腺细胞凋亡率显著高于安静组和力竭运动组 (P <0 . 0 5 ) ;训练 +力竭运动组脾细胞、外周血淋巴细胞内Ca2 +浓度及血清皮质醇浓度显著高于安静组 (P <0 . 0 5 ) ;力竭运动组血清皮质醇浓度亦显著高于安静组。结论 :耐力训练对力竭运动所诱导的血淋巴细胞凋亡有一定的抑制作用 ,对脾细胞凋亡无明显影响 ,还有增加胸腺细胞凋亡率的作用。耐力训练对力竭运动所诱导的血淋巴细胞及脾细胞凋亡的影响可能与阻断了细胞内Ca2 +浓度及血清C水平升高所介导的细胞凋亡信号转导有关。

Objective Effects of endurance swimming training on the exhaustion-induced lymphocyte apoptosis were investigated in rats and the mechanism was also analyzed. Methods Rats were randomly divided into sedentary group(S), exhaustive swimming group (ES) and endurance training plus exhaustive swimming group (ET). Before exhaustive swimming with 4% body weight loads started at the fourth week, rats in ET group enrolled in a 3-week endurance swimming training program. The apoptosis rates and the intracellular calcium concentration of splenocytes, thymocytes and peripheral blood lymphocytes as well as the serum cortisol levels were assayed right after exhaustive swimming. Results The swimming time of ET group lasted obviously longer than that of the ES group. In ET group, compared with ES group, the apoptosis rate of peripheral blood lymphocytes trended to decrease, the apoptosis rate of splenocytes was approximately equal and the apoptosis rate of thymocytes increased significantly. Moreover, the intracellular calcium concentration of splenocytes, peripheral blood lymphocytes and the serum cortisol levels in the ET group raised significantly compared with the S group. Meanwhile, the serum cortisol levels in the ES group were significantly higher than that of the S group. Conclusion Training could inhibit exhaustion-induced blood lymphocyte apoptosis and increase the thymocytes apoptosis rate, but had no certain effect on splenocyte apoptosis. Such effects were probably associated with inhibited intracellular calcium and serum cortisol from mediating apoptosis.