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有氧运动调节糖尿病大鼠海马突触可塑性相关蛋白表达的机制。

Mechanisms of Aerobic Exercise Upregulating the Expression of Hippocampal Synaptic Plasticity-Associated Proteins in Diabetic Rats.

机构信息

Shanghai University of Sport, Shanghai, China.

Brain and Spinal Cord Innovative Research Center, Tongji Hospital, Department of Physiology and Pharmacology, Tongji University School of Medicine, Shanghai, China.

出版信息

Neural Plast. 2019 Feb 18;2019:7920540. doi: 10.1155/2019/7920540. eCollection 2019.

DOI:10.1155/2019/7920540
PMID:30911292
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6398012/
Abstract

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 NFB/NLRP3/IL-1 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 NFB/NLRP3/IL-1 signaling pathway in the hippocampus of diabetic rats. Therefore, modulating the PI3K/Akt/mTOR, AMPK/Sirt1, and NFB/NLRP3/IL-1 signaling pathways is probably the mechanism of aerobic exercise upregulating the expression of hippocampal synaptic plasticity-associated proteins in diabetic rats.

摘要

我们研究了有氧运动对 2 型糖尿病大鼠海马突触可塑性相关蛋白表达的影响及其可能的机制。采用高脂饮食联合单次腹腔注射链脲佐菌素(STZ)建立 2 型糖尿病大鼠模型,随后进行为期 4 周的有氧运动干预。通过 Y 迷宫测试测量记忆性能。通过 Western blot 评估突触可塑性相关蛋白以及参与 PI3K/Akt/mTOR、AMPK/Sirt1 和 NF-B/NLRP3/IL-1 信号通路的蛋白的表达和活性。我们的结果表明,有氧运动促进了糖尿病大鼠海马中突触可塑性相关蛋白的表达。有氧运动还激活了糖尿病大鼠海马中的 PI3K/Akt/mTOR 和 AMPK/Sirt1 信号通路,并抑制了 NF-B/NLRP3/IL-1 信号通路。因此,调节 PI3K/Akt/mTOR、AMPK/Sirt1 和 NF-B/NLRP3/IL-1 信号通路可能是有氧运动上调糖尿病大鼠海马突触可塑性相关蛋白表达的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc4c/6398012/bc5b561e999d/NP2019-7920540.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc4c/6398012/5f037601a544/NP2019-7920540.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc4c/6398012/bf3804fe1265/NP2019-7920540.002.jpg
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