Isoliquiritigenin ameliorates advanced glycation end-products toxicity on renal proximal tubular epithelial cells

Chin Yi Lin, Yu Cheng Lin, Catherine Reena Paul, Dennis Jine Yuan Hsieh, Cecilia Hsuan Day, Ray Jade Chen, Chia Hua Kuo, Tsung Jung Ho, Marthandam Asokan Shibu, Chin Hu Lai, Tzu Ching Shih, Wei Wen Kuo, Chih Yang Huang

Research output: Contribution to journalArticlepeer-review

Abstract

Diabetic nephropathy is a serious chronic complication affecting at least 25% of diabetic patients. Hyperglycemia associated advanced glycation end-products (AGEs) increase tubular epithelial-myofibroblast transdifferentiation (TEMT) and extracellular matrix synthesis and thereby causes renal fibrosis. The chalcone isoliquiritigenin, found in many herbs of Glycyrrhiza family, is known for potential health-promoting effects. However, their effects on AGE-associated renal proximal tubular fibrosis are not known yet. In this study, the effect of isoliquiritigenin on AGE-induced renal proximal tubular fibrosis was determined in cultured HK-2 cell line. The results show that 200 μg/mL of AGE-induced TEMT and the formed myofibroblasts synthesized collagen to increase extracellular matrix formation thereby lead to renal tubular fibrosis. However, treatment with 200 nM of isoliquiritigenin considerably inhibited the TEMT and suppressed the TGFβ/STAT3 mechanism to inhibit collagen secretion. Therefore, isoliquiritigenin effectively suppressed AGE-induced renal tubular fibrosis.

Original languageEnglish
JournalEnvironmental Toxicology
DOIs
Publication statusAccepted/In press - 2022

Keywords

  • diabetic nephropathy
  • epithelial-myofibroblast transdifferentiation
  • fibrosis
  • radix Glycyrrhizae

ASJC Scopus subject areas

  • Toxicology
  • Management, Monitoring, Policy and Law
  • Health, Toxicology and Mutagenesis

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