抑制N-甲基-D-阿斯巴提酸受体可以防止肥胖引起的脏疾病
Àuria Eritja1, Catalina Pérez-Olives1, Dariel A Rodríguez Falcón1
1Vascular and Renal Translational Research Group, Institut de Recerca Biomèdica de Lleida - Fundació Dr Pifarré, IRBLleida, Lleida, Spain.
概括
N-甲基-D-酸盐受体 (NMDARs) 通过促进炎症和损伤,在肥胖引起的病中发挥关键作用. 向NMDAR可能为治疗这种疾病提供治疗策略.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 分子生物学分子生物学
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 与肥胖相关的脏病是一个越来越令人担忧的不清楚的分子机制.
- N-甲基-D-酸盐受体 (NMDARs) 与各种脏疾病有关.
- 这项研究调查了NMDAR在肥胖引起的病 (OIKD) 中的作用.
研究的目的:
- 阐明N-甲基-D-酸盐受体 (NMDARs) 在肥胖诱导脏疾病 (OIKD) 病变发生中的作用.
- 在OIKD中探索针对NMDARs的治疗潜力.
主要方法:
- 在OIKD小鼠模型,体外脂肪过载模型和人类脏活检中评估了NMDAR表达.
- 利用NMDAR对抗剂 (孟坦丁,MK-801),在HK-2细胞中获得和丧失功能的策略.
- 研究了p38酸化在FFA诱导的NMDAR上调中的作用.
主要成果:
- 在HK-2细胞和OIKD小鼠中增加的GluN1 (NMDAR子单元) 与脂质积累,炎症和细胞损伤相关.
- NMDAR对抗作用减少了FFA诱导的脂质积累,炎症,并改善了氧化还原平衡.
- 在体内NMDAR阻塞减少了炎症和管状损伤,增强了抗氧化剂基因表达.
- 在慢性病 (CKD) 患者的活检中观察到高GluN1水平.
结论:
- 脏NMDAR对肥胖诱导脏疾病 (OIKD) 的病原发生有显著的贡献.
- 向NMDAR证明了减轻肥胖相关脏病的炎症和损伤的治疗潜力.
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