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CAS No. : 1184-78-7
MCE 国际站:Trimethylamine N-oxide
产品活性:Trimethylamine N-oxide 是一种膳食胆碱和其他含三甲胺营养素的肠道微生物依赖性代谢产物。Trimethylamine N-oxide 通过激活 ROS/NLRP3 炎性体诱导炎症。Trimethylamine N-oxide 还通过激活 TGF-β/smad2 信号通路来加速成纤维细胞的分化并诱导心脏纤维化。
研究领域:Immunology/Inflammation | NF-κB | TGF-beta/Smad | Stem Cell/Wnt | Metabolic Enzyme/Protease
作用靶点:NOD-like Receptor (NLR) | Reactive Oxygen Species | TGF-beta/Smad | Endogenous Metabolite
结构分类:其他类 | 结构分类
In Vitro: The size and migration of fibroblasts are increased after Trimethylamine N-oxide (TMAO) treatment compared with non-treated fibroblasts in vitro. Trimethylamine N-oxide increases TGF-β receptor I expression, which promotes the phosphorylation of Smad2 and up-regulates the expression of α-SMA and collagen I. The ubiquitination of TGF-βRI is decreased in neonatal mouse fibroblasts after Trimethylamine N-oxide treatment. Trimethylamine N-oxide also inhibits the expression of smurf2.
Trimethylamine N-oxide is frequently found in the tissues of a variety of marine organisms that protects against the adverse effects of temperature, salinity, high urea and hydrostatic pressure.
In Vivo: Trimethylamine N-oxide can be used in animal modeling to construct models of cardiac fibrosis.
Trimethylamine N-oxide (TMAO) contributes to cardiovascular diseases by promoting inflammatory responses. C57BL/6 mice are fed a normal diet, high-choline diet and/or 3-dimethyl-1-butanol (DMB) diet. The levels of Trimethylamine N-oxide and choline are increased in choline-fed mice. Left ventricular hypertrophy, pulmonary congestion, and diastolic dysfunction are markedly exacerbated in heart failure with preserved ejection fraction (HFpEF) mice fed high-choline diets compared with mice fed the control diet. Myocardial fibrosis and inflammation were markedly increased in HFpEF mice fed high-choline diets compared with animals fed the control diet.
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