Background
Trimethylamine N-oxide (dihydrate) 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 (dihydrate) induced cardiac hypertrophy and cardiac fibrosis in SD rats[2].
Specific Mmodeling Methods
Rats: 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 (dihydrate) (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℃, 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 (dihydrate) 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 (dihydrate) on the inotropic and chronotropic effects. For the next seven days, the mice in the second group received Trimethylamine N-oxide (dihydrate) 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 (dihydrate) to the buffer solution increased the content of Trimethylamine N-oxide (dihydrate) in cardiac tissue by three and in the aortic rings by two points five times[1].
Pathology change: Trimethylamine N-oxide (dihydrate) 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 disease (CVD)[3].
Correlated Product(s):Isoproterenol (HY-B1670A)
3,3-dimethyl-1-butanol (HY-W012977)
