يثبط Salidroside مقاومة الأنسولين والتشحم الكبدي عن طريق تقليل تنظيم miR-21 والتفعيل اللاحق لـ AMPK وتنظيم PPAR? في الكبد والعضلات في الفئران التي تتغذى على نظام غذائي عالي الدهون

This study evaluated if salidroside (SAL) alleviates high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) by downregulating miR-21. Rats (n ? 8/group) were treated for 12 weeks as normal diet (control/ND), ND ? agmoir negative control (NC) (150 mg/kg), ND ? SAL (300 mg/kg), HFD, HFD ? SAL, HFD ? compound C (an AMPK inhibitor) (200 ng/kg), HFD? SAL? NXT629 (a PPAR-a antagonist) (30 mg/kg), and HFD? SAL? miR-21 agomir (150 mg/kg). SAL improved glucose and insulin tolerance and preserved livers in HFD-fed rats. In ND and HFD-fed rats, SAL reduced levels of serum and hepatic lipids and the hepatic expression of SREBP1, SREBP2, fatty acid (FA) synthase, and HMGCOAR. It also activated hepatic Nrf2 and increased hepatic/muscular activity of AMPK and levels of PPARa. All effects afforded by SAL were prevented by CC, NXT629, and miR-21 agmoir. In conclusion, activation of AMPK and upregulation of PPARa mediate the anti-steatotic effect of SAL.