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l-Carnitine Inhibits Lipopolysaccharide-Induced Nitric Oxide Production of SIM-A9 Microglia Cells
ACS Chemical Neuroscience ( IF 5 ) Pub Date : 2018-01-25 00:00:00 , DOI: 10.1021/acschemneuro.7b00468
Emily L. Gill 1 , Shreya Raman 2 , Richard A. Yost 1, 3 , Timothy J. Garrett 3 , Vinata Vedam-Mai 2
Affiliation  

Microglia are the resident immune effector cells of the central nervous system. They account for approximately 10–15% of all cells found in the brain and spinal cord, acting as macrophages, sensing and engaging in phagocytosis to eliminate toxic proteins. Microglia are dynamic and can change their morphology in response to cues from their milieu. Parkinson’s disease is a neurodegenerative disease, associated with reactive gliosis, neuroinflammation, and oxidative stress. It is thought that Parkinson’s disease is caused by the accumulation of abnormally folded alpha-synuclein protein, accompanied by persistent neuroinflammation, oxidative stress, and subsequent neuronal injury/death. There is evidence in the literature for mitochondrial dysfunction in Parkinson’s disease as well as fatty acid beta-oxidation, involving l-carnitine. Here we investigate l-carnitine in the context of microglial activation, suggesting a potential new strategy of supplementation for PD patients. Preliminary results from our studies suggest that the treatment of activated microglia with the endogenous antioxidant l-carnitine can reverse the effects of detrimental neuroinflammation in vitro.

中文翻译:

肉碱抑制脂多糖诱导的一氧化氮产生的SIM-A9小胶质细胞。

小胶质细胞是中枢神经系统的常驻免疫效应细胞。它们约占大脑和脊髓中所有细胞的10–15%,充当巨噬细胞,感知并参与吞噬作用以消除有毒蛋白质。小胶质细胞是动态的,可以根据环境的提示改变其形态。帕金森氏病是一种神经退行性疾病,与反应性神经胶质增生,神经炎症和氧化应激有关。认为帕金森氏病是由异常折叠的α-突触核蛋白蛋白的积累引起的,伴有持续的神经炎症,氧化应激和随后的神经元损伤/死亡。有在帕金森氏病中的文献对线粒体功能障碍证据以及脂肪酸β氧化,涉及-肉碱。这里,我们调查的小胶质细胞活化的背景下肉碱,提示补充的PD患者一个潜在的新策略。我们研究的初步结果表明,用内源性抗氧化剂l-肉碱治疗活化的小胶质细胞可以逆转体外有害的神经炎症的作用。
更新日期:2018-01-25
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