三甲胺-N-氧化物在动脉粥样硬化发病机制中的研究进展
发布时间：2018-12-27 18:37
【摘要】：肠道菌群的代谢产物三甲胺-N-氧化物(trimethylamine-N-oxide,TMAO)是一种新发现的心血管疾病的危险因子。肠道菌群利用食物中的胆碱和左旋肉碱转化为三甲胺(trimethylamine,TMA),三甲胺在肝酶中氧化为TMAO,降低TMA可以刺激巨噬细胞逆向转运胆固醇和抑制动脉粥样硬化形成。TMAO生成素单加氧酶3(flavin-containing monooxygenase 3,FMO3)是胆固醇代谢和胆固醇逆向转运的工具,降低FMO3可以减缓胆囊分泌胆汁,延缓肠道对胆固醇的吸收,并限制合成氧化型胆固醇和胆固醇酯。血液中TMAO可上调巨噬细胞内的清道夫受体,促使巨噬细胞内胆固醇累积和泡沫细胞的形成,进而促进血管斑块的形成并通过MAPK和细胞核因子κB通路促进血管炎性反应。TMAO集中作用于影响胆固醇代谢、胰岛素抵抗、促进血小板高聚集、增加血栓形成、促进血管炎症反应及直接导致动脉斑块形成等方面。降低TMAO水平可以潜在的预防或治疗动脉粥样硬化相关疾病,降低心脑血管疾病发病率。TMA/FMO3/TMAO通路是调节脂质代谢和炎症的主要通路。
[Abstract]:Trimethylamine-N-oxide (trimethylamine-N-oxide,TMAO), a metabolite of intestinal flora, is a new risk factor for cardiovascular disease. The intestinal flora uses choline and L-carnitine in food to convert to trimethylamine (trimethylamine,TMA), which is oxidized to TMAO, in the liver enzyme. Lowering TMA stimulates the reverse transport of cholesterol in macrophages and inhibits the formation of atherosclerosis. TMAO monooxygenase 3 (flavin-containing monooxygenase 3 FMO3) is a tool for cholesterol metabolism and cholesterol reverse transport. Lowering FMO3 can slow down gallbladder bile secretion, delay intestinal absorption of cholesterol, and limit the synthesis of oxidized cholesterol and cholesterol ester. TMAO in blood can up-regulate scavenger receptor in macrophages and promote cholesterol accumulation and foam cell formation in macrophages. In turn, it promotes the formation of vascular plaque and promotes vascular inflammatory response through MAPK and nuclear factor 魏 B. TMAO concentrates on affecting cholesterol metabolism, insulin resistance, platelet hyperaggregation and thrombus formation. Promote vascular inflammation and direct arterial plaque formation. Lowering the level of TMAO can potentially prevent or treat atherosclerotic diseases and reduce the incidence of cardiovascular and cerebrovascular diseases. TMA/FMO3/TMAO pathway is the main pathway to regulate lipid metabolism and inflammation.
【作者单位】： 广州中医药大学第二临床医学院神经内科;广东省中医院珠海医院神经内科;四川大学华西口腔医院特诊科;
【分类号】：R543.5
，
本文编号：2393449
[Abstract]:Trimethylamine-N-oxide (trimethylamine-N-oxide,TMAO), a metabolite of intestinal flora, is a new risk factor for cardiovascular disease. The intestinal flora uses choline and L-carnitine in food to convert to trimethylamine (trimethylamine,TMA), which is oxidized to TMAO, in the liver enzyme. Lowering TMA stimulates the reverse transport of cholesterol in macrophages and inhibits the formation of atherosclerosis. TMAO monooxygenase 3 (flavin-containing monooxygenase 3 FMO3) is a tool for cholesterol metabolism and cholesterol reverse transport. Lowering FMO3 can slow down gallbladder bile secretion, delay intestinal absorption of cholesterol, and limit the synthesis of oxidized cholesterol and cholesterol ester. TMAO in blood can up-regulate scavenger receptor in macrophages and promote cholesterol accumulation and foam cell formation in macrophages. In turn, it promotes the formation of vascular plaque and promotes vascular inflammatory response through MAPK and nuclear factor 魏 B. TMAO concentrates on affecting cholesterol metabolism, insulin resistance, platelet hyperaggregation and thrombus formation. Promote vascular inflammation and direct arterial plaque formation. Lowering the level of TMAO can potentially prevent or treat atherosclerotic diseases and reduce the incidence of cardiovascular and cerebrovascular diseases. TMA/FMO3/TMAO pathway is the main pathway to regulate lipid metabolism and inflammation.
【作者单位】： 广州中医药大学第二临床医学院神经内科;广东省中医院珠海医院神经内科;四川大学华西口腔医院特诊科;
【分类号】：R543.5
，
本文编号：2393449
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