Suppression of dimerumic acid on hepatic fibrosis caused from carboxymethyl-lysine (CML) by attenuating oxidative stress depends on Nrf2 activation in hepatic stellate cells (HSCs)

Bao Hong Lee, Wei Hsuan Hsu, Ya Wen Hsu, Tzu Ming Pan

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Hyperglycemia facilitates the formation of advanced glycation end-products (AGEs) in type-2 diabetes. Evidence indicates that carboxymethyl-lysine (CML) is highly prevalent in diabetes, resulting in hepatic fibrosis. The current study was designed to evaluate the effects of dimerumic acid (DMA) identified from Monascus-fermented products on receptor for AGEs (RAGE) signal and hepatic stellate cells (HSCs) activation by CML treatment. We found that DMA (50. μM) eliminated collagen generation, mRNA expressions of α-smooth muscle actin (α-SMA), platelet-derived growth factor-β receptor (PDGF-βR), and procollagen 1a1 (proCol-1a1) in CML (100. μg/ml)-treated HSCs, and these effects were similar to allyl isothiocyanate (AITC; 50. μM). In addition, the suppression of α-SMA, PDGF-βR, proCol-1a1 by DMA were abolished while nuclear factor-erythroid 2-related factor 2 (Nrf2) silence in CML-treated HSCs. These findings suggested that DMA and AITC increased Nrf2 and glutamate-cysteine ligase (GCL) activities thereby inhibiting oxidative stress caused by CML and showing anti-fibrogentic effect in HSCs.

Original languageEnglish
Pages (from-to)413-419
Number of pages7
JournalFood and Chemical Toxicology
Volume62
DOIs
Publication statusPublished - 2013 Dec

    Fingerprint

All Science Journal Classification (ASJC) codes

  • Food Science
  • Toxicology

Cite this