Open AccessDihydromyricetin Attenuates Streptozotocin‐induced Liver Injury and Inflammation in Rats via Regulation of NF‐ κ B and AMPK Signaling Pathway
Author(s) -
Chen Lei,
Yao Maojun,
Fan Xiaoyun,
Lin Xiujun,
Arroo Randolph,
Silva Aline,
Sungthong Bunleu,
Dragan Simona,
Paoli Paolo,
Wang Shaoyun,
Teng Hui,
Xiao Jianbo
Publication year - 2020
Publication title -
efood
Language(s) - English
Resource type - Journals
ISSN - 2666-3066
DOI - 10.2991/efood.k.200207.001
Subject(s) - ampk , streptozotocin , inflammation , oxidative stress , endocrinology , tlr4 , medicine , p38 mitogen activated protein kinases , diabetes mellitus , signal transduction , tumor necrosis factor alpha , apoptosis , liver injury , kinase , protein kinase a , pharmacology , chemistry , biochemistry
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‐1 β 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‐3 β 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.