Title : Involvement of CYP2E1-ROS-CD36/DGAT2 axis in the pathogenesis of VPA-induced hepatic steatosis in vivo and in vitro.

Pub. Date : 2020 Dec 1

PMID : 33007364






3 Functional Relationships(s)
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1 Importantly, VPA-induced ROS accumulation and hepatic steatosis were attenuated when CYP2E1 was inhibited using CYP2E1 inhibitor, diallyl sulfide (DAS, 100 mg/kg in mice, 1 mM in LO2 cells) or in CYP2E1-knockdown cell line, suggesting that CYP2E1 plays a potential role in ROS production following hepatic steatosis. allyl sulfide cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus
2 Importantly, VPA-induced ROS accumulation and hepatic steatosis were attenuated when CYP2E1 was inhibited using CYP2E1 inhibitor, diallyl sulfide (DAS, 100 mg/kg in mice, 1 mM in LO2 cells) or in CYP2E1-knockdown cell line, suggesting that CYP2E1 plays a potential role in ROS production following hepatic steatosis. allyl sulfide cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus
3 Importantly, VPA-induced ROS accumulation and hepatic steatosis were attenuated when CYP2E1 was inhibited using CYP2E1 inhibitor, diallyl sulfide (DAS, 100 mg/kg in mice, 1 mM in LO2 cells) or in CYP2E1-knockdown cell line, suggesting that CYP2E1 plays a potential role in ROS production following hepatic steatosis. allyl sulfide cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus