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首页> 外文期刊>Medicine and science in sports and exercise >Endurance Exercise Prevents Metabolic Distress-induced Senescence in the Hippocampus
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Endurance Exercise Prevents Metabolic Distress-induced Senescence in the Hippocampus

机译：耐力锻炼可以防止在海马中的代谢窘迫诱导衰老

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Purpose Metabolic disorder such as obesity and type 2 diabetes caused by excess caloric intake is associated with an increased risk of neurodegenerative diseases. Endurance exercise (EXE) has been suggested to exert neuroprotective effects against the metabolic distress. However, the exact underlying molecular mechanisms responsible for the exercise-induced neuroprotection have not been fully elucidated. In this study, we investigated whether EXE-induced neuroprotection is associated with cellular senescence, neuroinflammation, and oxidative stress using a mouse model of obesity induced by a high-fat/high-fructose diet. Methods C57BL/6 female mice (10 wk old) were randomly divided to three groups: normal chow diet group (CON, n = 11), high-fat diet/high-fructose (HFD/HF) group (n = 11), and high-fat diet/high-fructose + endurance exercise (HFD/HF + EXE) group (n = 11). HFD/HF + EXE mice performed treadmill running exercise for 60 min center dot d(-1), 5 d center dot wk(-1) for 12 wk. Results Our data showed that EXE ameliorated HFD/HF-induced weight gain, fasting blood glucose levels, and visceral fat gain. More importantly, HFD/HF diet promoted cellular senescence, whereas EXE reversed it, evidenced by a reduction in the levels of p53, p21, p16, beta-galactosidase (SA-beta-gal), and lipofuscin. Furthermore, EXE prevented HFD/HF-induced neuroinflammation (e.g., tumor necrosis factor-alpha and interleukin-1 beta) by inhibiting toll-like receptor 2 downstream signaling cascades (e.g., tumor necrosis factor receptor-associated factor 6, c-Jun N-terminal kinase, and c-Jun) in parallel with reduced reactive glial cells. This anti-inflammatory effect of EXE was associated with the reversion of HFD/HF-induced cellular oxidative stress. Conclusion Our study provides novel evidence that EXE-induced antisenescence against metabolic distress in the hippocampus may be a key neuroprotective mechanism, preventing neuroinflammation and oxidative stress.
机译：目的代谢障碍如肥胖症和由过量的热量摄入量引起的2型糖尿病与神经变性疾病的风险增加有关。已经提出了耐力运动（EXE）对代谢窘迫发挥神经保护作用。然而，尚未完全阐明负责运动诱导的神经保护的确切潜在的分子机制。在这项研究中，我们研究了exe诱导的神经保护术与使用高脂/高果糖饮食诱导的肥胖小鼠模型与细胞衰老，神经炎炎症和氧化应激相关。方法C57BL / 6雌性小鼠（10WK旧）随机分为三组：正常分号饮食组（CON，N = 11），高脂饮食/高果糖（HFD / HF）组（n = 11），和高脂饮食/高果糖+耐久性运动（HFD / HF + EXE）组（n = 11）。 HFD / HF + EXE小鼠对60分钟中心点D（-1），5 d中心点WK（-1）进行了12周的跑步机运行锻炼。结果我们的数据显示，EXE改善了HFD / HF诱导的体重增加，空腹血糖水平和内脏脂肪增益。更重要的是，HFD / HF饮食促进了细胞衰老，而exe逆转，则通过降低P53，P21，P16，β-半乳糖苷酶（SA-Beta-Gal）和Lipofuscin的水平减少证明。此外，通过抑制可收费的受体2下游信号级联（例如，肿瘤坏死因子受体相关因子6，C-Jun N，通过抑制Toll样受体2（例如，肿瘤坏死因子受体相关因子6，C-Jun N - 寿命激酶和C-Jun）与降低的活性胶质细胞平行。 EXE的这种抗炎作用与HFD / HF诱导的细胞氧化应激的逆转有关。结论我们的研究提供了新的证据，即epe诱导的海马在海马中代谢窘迫的抗血糖可能是一种关键的神经保护机制，预防神经炎症和氧化应激。

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