Magnesium trihydrate ((S)-Omeprazole magnesium trihydrate) is a potent and orally active H+, K+-ATPase inhibitor. Esomeprazole magnesium trihydrate demonstrates promise in the research of upper intestinal disorders and gastroesophageal reflux disease[1].[2]. Through the suppression of V-H+-ATPases, Esomeprazole magnesium trihydrate functions as an inhibitor of exosomes, preventing their release[4].
体内研究
Treatment with Esomeprazole magnesium (0.5-50 mg/kg; orally via gavage; daily; over 10 days; in A/J mice) leads to an enhancement in gastric total antioxidant capacity and the activity of Cu/Zn-superoxide dismutase[1].
体外研究
Esomeprazole magnesium trihydrate was developed from Esomeprazole strontium tetrahydrate (EST), which includes esomeprazole, the S-enantiomer of omeprazole, and represents a salt-exchanged form of Esomeprazole magnesium trihydrate[2].
Esomeprazole magnesium trihydrate/埃索美拉唑镁三水合物 细胞实验
Cell Line
Concentration
Treated Time
Description
References
primary human umbilical vein endothelial cells (HUVECs)
100 μmol/L
24 hours
Esomeprazole MH reduced sFLT-1 secretion, but MTH had no significant effect
Int J Mol Sci. 2022 Aug 23;23(17):9533
primary cytotrophoblast cells
100 μmol/L
24 hours
Reduced secretion of sFLT-1 and mRNA expression of sFLT1-e15a and sFLT1-i13
Int J Mol Sci. 2022 Aug 23;23(17):9533
Esomeprazole magnesium trihydrate/埃索美拉唑镁三水合物 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
L-NAME-induced hypertension model
Intraperitoneal injection
10 mg/kg
Daily from D7.5 to D17.5 of pregnancy
To assess the effect of esomeprazole on L-NAME-induced hypertension model, results showed esomeprazole did not lower blood pressure but enhanced ex vivo acetylcholine-induced vasorelaxation in obese mice.
Int J Mol Sci. 2022 Jul 25;23(15):8185
Sprague Dawley (SD) rats
Water-immersed and restraint (WIR)-induced stress ulcer model
Intraperitoneal injection
High dose 50 mg/kg/day, low dose 10 mg/kg/day
Once daily for 7 days
Esomeprazole pretreatment alleviates WIR-induced stress ulcer damage by inhibiting gastric acid secretion, exerting antioxidant and anti-inflammatory effects, and inactivating the p38 MAPK and NF-κB signaling pathways.
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