有氧训练对衰老小鼠快缩型骨骼肌蛋白质降解的抑制作用研究

关键词：有氧训练  衰老  骨骼肌  蛋白质降解

Keywords:aerobic exercise training  aging  skeletal muscle  protein degradation

摘要：

      摘要 目的：探讨规律有氧训练对衰老小鼠骨骼肌蛋白质降解的影响。 方法：17月龄雄性C57BL/6小鼠18只据体重随机纳入对照组（C组）与有氧训练组（AE组）。训练组小鼠以自身体重2.5%的负荷进行8周游泳训练，每周训练6天，每天1次，每次45min。末次训练24h后处死全部小鼠，禁食6h。酶联免疫吸附测定血清TNF-α、IL-1β和IL-6含量，荧光法检测类糜蛋白酶与钙蛋白酶活性，对硝基苯磷酸底物法检测酸性磷酸酶活性，免疫印迹法检测泛素蛋白酶体系统关键蛋白Atrogin-1、MuRF-1、Ubquitin及钙蛋白酶系μ-Calpain表达，色谱法检测腓肠白肌内3-MH含量。 结果：8周有氧训练可致衰老小鼠腓肠白肌促炎细胞因子含量、类糜蛋白酶与钙蛋白酶活性、3-MH含量以及Atrogin-1、MuRF-1、Ubquitin与μ-Calpain蛋白表达显著下降，且变化具有显著性意义（P=0.000）。但溶酶体酶活性未见组间差异。 结论：有氧训练可削弱衰老小鼠快缩型骨骼肌蛋白质降解，可能具有防治衰老性肌肉萎缩发生发展的潜力，其作用机制可能与其削弱炎性细胞因子生成集聚，进而抑制泛素蛋白酶体与钙蛋白酶系统的活性有关。

Abstract:

      Abstract Objective: To explore the effect of regularly aerobic exercise training on protein degradation of skeletal muscle in aging mice. Method: Eighteen seventeen-month-old male C57/BL mice were randomly divided into control group and aerobic exercise training group by body weight. Mice in training group received 8 wks moderate swimming training with 2.5% body weight workload, 45mins per day, 6 days per wk. Twenty-four hours after the final exercise bout (6h fasting), mice in both groups were sacrificed. The content of TNF-α, IL-1β and IL-6 in serum were measured with commercial ELISA kit. The chymotrypsin-like enzyme and calpain activity was detected by using fluorescence method. The acid phosphatase activity was measured with para-nitrophenyl phosphate method. The expression of Atrogin-1, MuRF-1, Ubiquitin and μ-Calpain was detected with Western blotting. The content of 3-MH in white gastrocnemius muscle was measured by means of chromatography. Result: When compared with mice in control group, 8 wks swimming exercise training decreased the content of pro-inflammatory cytokines in serum, the chymotrypsin-like enzyme and calpain activity, the content of 3-MH and the expression of Atrogin-1, MuRF-1, Ubiquitin and μ-Calpain with statistical significance (P=0.000). While there was no difference of acid phosphatase activity between groups. Conclusion: Aerobic exercise training attenuates the protein degradation in white gastrocnemius of aging mice. The diminished production and accumulation of pro-inflammatory cytokines, and then the secondary inhibition of both ubiquitin-proteasome and calpain activity may contribute to this function. These results suggest that aerobic exercise training may play a potentially potent role in ameliorating aging-related sarcopenia.