Abstract Title:

Xanthohumol alleviated T2DM-induced liver steatosis and fibrosis by mediating the NRF2/RAGE/NF-κB signaling pathway.

Abstract Source:

Future Med Chem. 2021 Sep 23. Epub 2021 Sep 23. PMID: 34551612

Abstract Author(s):

Wei Wang, Zhixi Chen, Tiansheng Zheng, Ming Zhang

Article Affiliation:

Wei Wang


Hyperglycemia-associated advanced glycation end products (AGEs) and the receptor for AGE (RAGE) contribute to nonalcoholic fatty liver disease (NAFLD). Xanthohumol (XH) exhibits protective activities against liver diseases.To investigate the effects of XH on Type II diabetes mellitus (T2DM)-induced liver steatosis and fibrosis.NAFLD rat models were duplicated. Biomolecular markers were detected. Quantitative real-time polymerase chain reaction (RT-PCR) and western blot were used to detect mRNA and protein expression. Immunofluorescence assays were employed to identify the subcellular locations.XH significantly ameliorated hyperglycemia and hyperlipidemia in rats. XH attenuated the expression of RAGE and NF-κB signaling. XH significantly alleviated inflammation and oxidation by upregulating NRF2 expression. Knockdown of NRF2 blocked XH protection in hepatocytes.XH protected against T2DM-induced liver steatosis and fibrosis by mediating NRF2/AGE/RAGE/NF-κB signaling.

Print Options

Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2022 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.