Dihydromyricetin Attenuates Streptozotocin-induced Liver Injury and Inflammation in Rats via Regulation of NF-κB and AMPK Signaling Pathway

Abstract

Dihydromyricetin (DHM) dramatically improved the quality of life for Streptozotocin (STZ)-induced diabetic rats and significantly increased the activity of antioxidant enzymes in the liver. Moreover, DHM successfully ameliorated diabetes-induced liver damage by suppression of apoptosis in the liver, as indicated by the decreased levels of Bax and cleaved caspase-3. In diabetic rats, the levels of tumor necrosis factor-α and interleukin-1β in the liver were significantly increased. However, the administration of DHM (100–400 mg/kg/day) for 6 weeks restored the cytokine levels to their normal values in a dose-dependent manner in diabetic rats by the regulation of nuclear factor-kappa B signaling pathway. In addition, DHM significantly induced 5′ AMP-activated protein kinase (AMPK) phosphorylation and decreased MyD88, TLR4, p38, GSK-3β protein expression levels in the liver of diabetic rats. In conclusion, DHM could improve STZ-induced liver impairment by preventing oxidative stress, apoptosis, and inflammation.

Keywords

• Ampelopsin
• AMPK
• diabetes
• dihydromyricetin
• inflammation
• liver-protective effects