Rilmenidine improves hepatic steatosis through p38-dependent pathway to higher the expression of farnesoid X receptor.

摘要: The nuclear receptor farnesoid X (FXR) regulates pathways in lipid, glucose, and energy metabolism. Activation of FXR mice significantly improved high-fat diet-induced hepatic steatosis. It has been reported that activation imidazoline I-1 by rilmenidine increases the expression human hepatoma cell line, Hep G2 cell, to regulate target genes relating lipid metabolism; exerts an antihyperlipidemic action. However, signals for this action are still unknown. In present study, steatosis induced diet was after intraperitoneal injection at 1 mg/kg daily 12 weeks. Also, mediation receptors identified using specific antagonist efaroxan. Moreover, decreased oleic acid-induced accumulation cells. Otherwise, increased phosphorylation p38 increase FXR. Deletion calcium ions BAPTA-AM reversed rilmenidine-induced phosphorylation. conclusion, we suggest activates intracellular may enhance higher improvement both animals