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首页> 外文期刊>Journal of Neural Transplantation and Plasticity: Neural Plasticity >Mechanisms of Aerobic Exercise Upregulating the Expression of Hippocampal Synaptic Plasticity-Associated Proteins in Diabetic Rats
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Mechanisms of Aerobic Exercise Upregulating the Expression of Hippocampal Synaptic Plasticity-Associated Proteins in Diabetic Rats

机译:有氧运动的机制上调糖尿病大鼠海马突触塑性相关蛋白的表达

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We investigated the effects of aerobic exercise on the expression of hippocampal synaptic plasticity-associated proteins in rats with type 2 diabetes and their possible mechanisms. A type 2 diabetes rat model was established with 8 weeks of high-fat diet combined with a single intraperitoneal injection of streptozotocin (STZ). Then, a 4-week aerobic exercise intervention was conducted. Memory performance was measured with Y maze tests. The expression and activity of synaptic plasticity-associated proteins and of proteins involved in the PI3K/Akt/mTOR, AMPK/Sirt1, and NFκB/NLRP3/IL-1β signaling pathways were evaluated by western blot. Our results show that aerobic exercise promotes the expression of synaptic plasticity-associated proteins in the hippocampus of diabetic rats. Aerobic exercise also activates the PI3K/Akt/mTOR and AMPK/Sirt1 signaling pathways and inhibits the NFκB/NLRP3/IL-1β signaling pathway in the hippocampus of diabetic rats. Therefore, modulating the PI3K/Akt/mTOR, AMPK/Sirt1, and NFκB/NLRP3/IL-1β signaling pathways is probably the mechanism of aerobic exercise upregulating the expression of hippocampal synaptic plasticity-associated proteins in diabetic rats.
机译:我们调查了有氧运动对2只糖尿病大鼠海马突触可塑性相关蛋白的影响及其可能的机制。 2型糖尿病大鼠模型是用8周的高脂饮食建立,结合单腹腔内注射链脲佐菌素(STZ)。然后,进行了4周的有氧运动干预。用Y迷宫测试测量内存性能。通过Western印迹评估突触塑性相关蛋白和参与PI3K / AKT / MTOR,AMPK / SIRT1和NFκB/ NLRP3 / IL-1β信号传导途径的蛋白质的表达和活性。我们的研究结果表明,有氧运动促进糖尿病大鼠海马突触塑性相关蛋白的表达。有氧运动也激活PI3K / AKT / MTOR和AMPK / SIRT1信号通路,并抑制糖尿病大鼠海马的NFκB/ NLRP3 / IL-1β信号通路。因此,调节PI3K / AKT / mTOR,AMPK / SIRT1和NFκB/ NLRP3 / IL-1β信号通路可能是有氧运动的机制上调糖尿病大鼠中海马突触塑性相关蛋白的表达。

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