Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China; Guangxi Normal University for Nationalities, Chongzuo, China.
Department of Clinical Medicine, Weifang Medical University, Weifang, China; Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China.
Brain Res Bull. 2018 Jun;140:52-59. doi: 10.1016/j.brainresbull.2018.04.003. Epub 2018 Apr 6.
Studies have shown high fat diet induced obesity may cause cognition impairment and down-regulation of neuroplasticity-associated proteins, while aerobic exercise could improve that damage. Endoplasmic reticulum stress (ERS) has been reported to play a key role in regulating neuroplasticity-associated proteins expression, folding and post-translational modification in hippocampus of obese rodent models, however, the effects of ERS on neuroplasticity-associated proteins and possible underlying mechanisms in prefrontal cortex are not fully clear. In order to clarify changes of neuroplasticity-associated proteins and ERS in the prefrontal cortex of obese rats, male SD rats were fed on high fat diet for 8 weeks to establish the obese model. Then, 8 weeks of aerobic exercise treadmill intervention was arranged for the obese rats. Results showed that high fat diet induced obesity caused hyperlipidemia, and significantly promoted FATP1 expression in the prefrontal cortex, meanwhile, we found up-regulation of GRP78, p-PERK, p-eIF2α, caspase-12, CHOP, and Bax/Bcl-2, reflecting the activation of ERS and ERS-mediated apoptosis. Moreover, reduced BDNF and SYN was found in obese rats. However, FATP1, GRP78, p-PERK, p-eIF2α, caspase-12, CHOP, and Bax/Bcl-2 expressions were obviously reversed by aerobic exercise intervention. These results suggested that dietary obesity could induce Prefrontal ERS in SD rats and excessive ERS may play a critical role in decreasing the levels of neuroplasticity-associated proteins. Moreover, aerobic exercise could relieve ERS, thus promoted the expression of neuroplasticity-associated proteins.
研究表明，高脂肪饮食诱导的肥胖可能导致认知障碍和神经可塑性相关蛋白的下调，而有氧运动可以改善这种损伤。内质网应激（ERS）已被报道在调节肥胖啮齿动物模型海马体中的神经可塑性相关蛋白的表达、折叠和翻译后修饰中发挥关键作用，然而，ERS 对前额叶皮质中神经可塑性相关蛋白的影响及其潜在机制尚不完全清楚。为了阐明肥胖大鼠前额叶皮质中神经可塑性相关蛋白和 ERS 的变化，雄性 SD 大鼠喂食高脂肪饮食 8 周建立肥胖模型。然后，对肥胖大鼠进行 8 周的有氧运动跑台干预。结果表明，高脂肪饮食诱导的肥胖导致高脂血症，并显著促进了前额叶皮质中 FATP1 的表达，同时，我们发现 GRP78、p-PERK、p-eIF2α、caspase-12、CHOP 和 Bax/Bcl-2 的上调，反映了 ERS 的激活和 ERS 介导的细胞凋亡。此外，肥胖大鼠中 BDNF 和 SYN 减少。然而，有氧运动干预明显逆转了 FATP1、GRP78、p-PERK、p-eIF2α、caspase-12、CHOP 和 Bax/Bcl-2 的表达。这些结果表明，饮食肥胖可诱导 SD 大鼠前额叶 ERS，过度的 ERS 可能在降低神经可塑性相关蛋白水平中发挥关键作用。此外，有氧运动可以缓解 ERS，从而促进神经可塑性相关蛋白的表达。
