在肥胖相关的神经炎症中调节TLR4/MAPK/ROS信号的治疗前景
Drashti Sharma1, Ram Narayanan Ravi2, Amar Daud Iskandar Abdullah1
1Department of Biomedical Sciences, Sir Jeffrey Cheah Sunway Medical School, Faculty of Medical and Life Sciences, Sunway University, Malaysia.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|November 28, 2025
概括
肥胖导致慢性炎症,影响大脑健康,增加神经退行性疾病的风险. 针对炎症途径为与肥胖相关的大脑功能障碍提供了潜在的治疗策略.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 肥胖越来越被认为是一种慢性炎症状况,影响代谢健康和大脑功能.
- 由脂肪组织扩张引起的系统性炎症会损害血脑屏障 (BBB),促进免疫细胞透和与中枢神经系统 (CNS) 通信.
研究的目的:
- 阐明将肥胖引起的外周炎症与中枢神经系统 (CNS) 免疫激活和神经炎症联系起来的分子机制.
- 确定关键途径和分子点,以减轻肥胖驱动的神经炎症及其相关的神经后果.
主要方法:
- 关于参与肥胖相关炎症的分子途径的审查,包括巨细胞两极分化,细胞因子释放和肠道衍生因素.
- 在中枢神经系统中激活托尔类受体4 (TLR4),核因子-κB (NF-κB) 和基激活蛋白激酶 (MAPK) 级联的激活分析.
- 检查线粒体功能障碍,氧化应激,活性氧物种 (ROS) 和NLRP3炎症体在质细胞激活中的作用.
主要成果:
- 肥胖会引发系统性炎症,从而削弱BBB,使外周炎症信号能够激活中枢神经系统通路,如TLR4,NF-κB和MAPK.
- 线粒体功能障碍和氧化应激通过激活NLRP3炎症酶和促进质细胞过活化,加剧神经炎症.
- 这些神经炎症过程有助于突触功能障碍,神经元对胰岛素的抵抗,以及对神经退行性疾病 (如阿尔茨海默氏症和帕金森病) 的脆弱性增加.
结论:
- 肥胖驱动的神经炎症涉及周围代谢失调和中央免疫反应之间的复杂相互作用.
- 准关键的炎症介质 (TLR4,MAPK) 和氧化应激通路 (ROS,NLRP3) 是一个有前途的治疗途径.
- 了解代谢-炎症-神经元轴对于开发有效的干预措施来预防与肥胖相关的神经衰退至关重要.
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