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目的:研究不同强度的耐力训练对糖尿病大鼠骨骼肌细胞丝裂素活化蛋白激酶p38活性的调节作用,为制订适宜的糖尿病运动疗法程序提供分子生物学依据。方法:雄性SD大鼠34只,尾静脉注射链脲霉素,建立糖尿病模型。然后随机分为低强度运动组(E1,n=6)、高强度运动组(E2,n=6)、低强度运动加胰岛素治疗组(EI1,n=6)、高强度运动加胰岛素治疗组(EI2,n=6)、非胰岛素治疗非运动组(C,n=5)和胰岛素治疗非运动组(CI,n=5)。耐力训练采用活动平板,胰岛素皮下注射,共8周。运用化学发光法测定p38活性。结果:训练8周前后,EI1组安静血糖下降46%(P<0.01),其余各组血糖无明显下降。单次运动前后E1组、EI1组、EI2组和CI组血糖均见明显下降,其中EI1组血糖降低尤为显著达83%(P<0.01)。骨骼肌p38活性在EI1组显著高于其余各组(P<0.05),E1组显著高于E2组、C组、CI组(P<0.05)。结论:低强度运动训练以及低强度运动训练加胰岛素治疗均能显著提高糖尿病大鼠骨骼肌细胞p38信号激酶,提示低强度运动训练加胰岛素治疗是内源性胰岛素缺乏性糖尿病的适宜治疗方案。
OBJECTIVE: To study the regulatory effect of endurance training with different intensities on the activity of mitogen-activated protein kinase p38 in skeletal muscle cells of diabetic rats and to provide a molecular biological basis for the development of appropriate exercise programs. Methods: Thirty-four male Sprague-Dawley rats were injected with streptozotocin through tail vein to establish a model of diabetes mellitus. And then randomly divided into low intensity exercise group (E1, n = 6), high intensity exercise group (E2, n = 6), low intensity exercise plus insulin treatment group (EI1, n = 6), high intensity exercise plus insulin treatment group (EI2, n = 6), non-insulin treatment non-exercise group (C, n = 5) and insulin treatment non-exercise group (CI, n = 5). Endurance training using active plate, subcutaneous insulin injection, a total of 8 weeks. Determination of p38 activity by chemiluminescence method. Results: Before and after the training, the quiet blood glucose in EI1 group decreased 46% (P <0.01), while the other groups had no obvious decrease in blood glucose. Before and after single exercise, the levels of blood glucose in E1, EI1, EI2 and CI groups were significantly decreased, especially in EI1 group was 83% (P <0.01). The p38 activity of skeletal muscle in EI1 group was significantly higher than that in other groups (P <0.05), while E1 group was significantly higher than E2 group, C group and CI group (P <0.05). CONCLUSION: Low-intensity exercise training and low-intensity exercise training combined with insulin therapy can significantly increase p38 signaling kinase in skeletal muscle cells of diabetic rats, suggesting that low-intensity exercise training and insulin therapy are suitable treatment options for endogenous insulin-deficient diabetes.