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- Title
Isoliquiritigenin ameliorates advanced glycation end‐products toxicity on renal proximal tubular epithelial cells.
- Authors
Lin, Chin‐Yi; Lin, Yu‐Cheng; Paul, Catherine Reena; Hsieh, Dennis Jine‐Yuan; Day, Cecilia Hsuan; Chen, Ray‐Jade; Kuo, Chia‐Hua; Ho, Tsung‐Jung; Shibu, Marthandam Asokan; Lai, Chin‐Hu; Shih, Tzu‐Ching; Kuo, Wei‐Wen; Huang, Chih‐Yang
- 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.
- Subjects
ADVANCED glycation end-products; NEPHROTOXICOLOGY; RENAL fibrosis; MYOFIBROBLASTS; EPITHELIAL cells; HYPERGLYCEMIA; DIABETIC nephropathies; CHALCONE
- Publication
Environmental Toxicology, 2022, Vol 37, Issue 8, p2096
- ISSN
1520-4081
- Publication type
Article
- DOI
10.1002/tox.23553