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Nuclear Factor [Erythroid-derived 2]-like 2 and Mitochondrial Transcription Factor A Contribute to Moderate-intensity Swimming Effectiveness against Memory Impairment in Young Mice Induced by Concomitant Exposure to a High-calorie Diet during the Early Life Period
Neuroscience ( IF 3.3 ) Pub Date : 2020-11-24 , DOI: 10.1016/j.neuroscience.2020.11.023
Natália Silva Jardim 1 , Sabrina Grendene Müller 1 , Flávia Matos Pase 1 , Cristina Wayne Nogueira 1
Affiliation  

Increased energy food consumption during early-life has been associated with memory impairment. Swimming training has been reported to improve memory processes in rodent models. This study aimed to evaluate whether moderate-intensity swimming training counteracts learning and memory impairment in young mice fed a high-calorie diet during the early-life period. The contribution of hippocampal oxidative stress, as well as nuclear factor [erythroid-derived 2]-like 2/Kelch-like ECH-associated protein (NRF2/Keap-1/HO-1) and peroxisome proliferator-activated receptor gamma co-activator 1-alpha/mitochondrial transcription factor A (PCG-1α/mtTFA) signaling, in memory effects was also investigated. Three-week-old male Swiss mice received a high-calorie diet (20% fat; 20% carbohydrate enriched) or a standard diet from 21 to 49 postnatal days. Mice performed a moderate-intensity swimming protocol (5 days/week) and behavioral tests predictive of memory function. Mice fed a high-calorie diet and subjected to the swimming protocol performed better on short- and long-term spatial and object recognition memory tests than those fed a high-calorie diet. The swimming protocol modulated the hippocampal NRF2/Keap-1/HO-1 and mtTFA pathways in mice fed a high-calorie diet. Swimming training positively affected location and long-term memory, fat mass content, as well as NRF2/Keap-1/HO-1 and mtTFA proteins of control‐diet‐fed mice. In conclusion, a moderate-intensity swimming training evoked an adaptive response in mice fed a high-calorie diet by restoring different types of memory-impaired and hippocampal oxidative stress as well as upregulated the NRF2/Keap-1/HO-1 and mtTFA pathways.



中文翻译:

核因子 [红细胞衍生 2] 样 2 和线粒体转录因子 A 有助于中等强度游泳对早期同时暴露于高热量饮食引起的年轻小鼠记忆障碍的有效性

生命早期能量食物消耗的增加与记忆障碍有关。据报道,游泳训练可以改善啮齿动物模型的记忆过程。本研究旨在评估中等强度游泳训练是否能抵消在生命早期喂食高热量饮食的年轻小鼠的学习和记忆障碍。海马氧化应激的贡献,以及核因子 [红细胞衍生 2] 样 2/Kelch 样 ECH 相关蛋白 (NRF2/Keap-1/HO-1) 和过氧化物酶体增殖物激活受体 γ 共激活剂还研究了记忆效应中的 1-α/线粒体转录因子 A (PCG-1α/mtTFA) 信号传导。三周大的雄性瑞士小鼠在出生后 21 至 49 天接受高热量饮食(20% 脂肪;20% 富含碳水化合物)或标准饮食。小鼠执行中等强度游泳方案(5 天/周)和预测记忆功能的行为测试。喂食高热量饮食并接受游泳方案的小鼠在短期和长期空间和物体识别记忆测试中的表现优于喂食高热量饮食的小鼠。游泳方案调节了喂食高热量饮食的小鼠的海马 NRF2/Keap-1/HO-1 和 mtTFA 通路。游泳训练对控制饮食喂养小鼠的位置和长期记忆、脂肪量以及 NRF2/Keap-1/HO-1 和 mtTFA 蛋白有积极影响。总之,中等强度游泳训练通过恢复不同类型的记忆受损和海马氧化应激以及上调 NRF2/Keap-1/HO-1 和 mtTFA 通路,在喂食高热量饮食的小鼠中引起了适应性反应.

更新日期:2020-12-09
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