MedChemExpress - Model Trimethylamine N-oxide -1184-78-7
Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway[1][2][3].MCE products for research use only. We do not sell to patients.
Trimethylamine N-oxide
MCE China：Trimethylamine N-oxide
Brand：MedChemExpress (MCE)
Cat. No.HY-116084
CAS：1184-78-7
Purity：98.0%
Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Shipping：Room temperature in continental US; may vary elsewhere.
Description：Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway.
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[2]. 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[3].
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[1].
IC50 & Target：NLRP3 Microbial Metabolite Human Endogenous Metabolite
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References：
[1]. Wei Shuai, et al. High-choline Diet Exacerbates Cardiac Dysfunction, Fibrosis, and Inflammation in a Mouse Model of Heart Failure With Preserved Ejection Fraction. J Card Fail. 2020 May 14;S1071-9164(19)31802-0. [Content Brief]
[2]. Wenlong Yang, et al. Gut Microbe-Derived Metabolite Trimethylamine N-oxide Accelerates Fibroblast-Myofibroblast Differentiation and Induces Cardiac Fibrosis. J Mol Cell Cardiol. 2019 Sep;134:119-130. [Content Brief]
[3]. Manuel T Velasquez, et al. Trimethylamine N-Oxide: The Good, the Bad and the Unknown. Toxins (Basel). 2016 Nov 8;8(11):326. [Content Brief]
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