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Trimethylamine N-oxide


CAS No. : 1184-78-7

1184-78-7
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Cat. No. : HY-116084
M.Wt: 75.11
Formula: C3H9NO
Purity: >98 %
Solubility: H2O : 100 mg/mL (ultrasonic);DMSO : 100 mg/mL (ultrasonic)
Introduction of 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]. IC50 & Target:ROS/NLRP3 inflammasome[1]
TGF-β/smad2[1] 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:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Trimethylamine N-oxide can be used in animal modeling to create cardiovascular and metabolic disease models[1].

Induction of cardiovascular and metabolic diseases
Background
Trimethylamine N-oxide stimulated cardiac hypertrophy, as indicated by increased cell area of cardiomyocytes and expression of hypertrophic markers including atrial natriuretic peptide (ANP) and beta-myosin heavy chain (β-MHC). Additionally, Trimethylamine N-oxide induced cardiac hypertrophy and cardiac fibrosis in SD rats[2].
Specific Mmodeling Methods
Rat: Wistar• male• weighing 200-250 g[1]
Administration: 100 μM and 1 mM• perfusion or incubation in TMAO-containing buffer solution• incubated for 1 h[1]
Mice: CD-1• male• weighing 25-30 g• 6-8 weeks of age[1]
Administration: 120 mg/kg• mixed with drinking water• a single dose or daily for 7 days[1]
Note
(1) Rat hearts were perfused, and aortic rings from each experimental animal were immersed in K+-H+ buffer solution with or without the addition of Trimethylamine N-oxide (100 μM final concentration). After 1 h of perfusion or incubation, the tissue samples were washed to eliminate the residues of TMAO-containing buffer solution and further homogenized with water in an OMNI Bead Ruptor 24 at a w/v ratio of 1:10[1].
(2) All experimental animals were housed under standard conditions (21-23°C, 12-hour light/dark cycle, relative humidity 45-65%) with unlimited access to food (R70 diet) and water[1].
(3) The mice from the first experimental group received Isoproterenol (HY-B1670A) at a dose of 10 μg/mouse, but the animals from the second group received Isoproterenol (HY-B1670A) and Trimethylamine N-oxide at doses of 10 μg/mouse and 120 mg/kg, respectively. After 30 min, the experimental animals were anesthetized with isoflurane once more to record the cardiac response to acute cardiac stress and the impact of Trimethylamine N-oxide on the inotropic and chronotropic effects. For the next seven days, the mice in the second group received Trimethylamine N-oxide together with drinking water at a dose of 120 mg/kg, while the animals from the first group received pure drinking water[1].
Modeling Indicators
Molecular changes: The addition of 100 μM Trimethylamine N-oxide to the buffer solution increased the content of Trimethylamine N-oxide in cardiac tissue by three and in the aortic rings by two points five times[1].
Pathology change: Trimethylamine N-oxide had no influence on Isoproterenol (HY-B1670A)-induced increase on left ventricular ejection fraction, fractional shortening and heart rate[1].
Histological analysis: Promote myocardial hypertrophy, fibrosis, and inflammation in a model of cardiovascular diseases (CVDs)[3].
Correlated Product(s): Isoproterenol (HY-B1670A)
Opposite Product(s): 3,3-dimethyl-1-butanol (HY-W012977)

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