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

doi:10.1002/tox.23553

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

外科學科

研究成果: 雜誌貢獻 › 文章 › 同行評審

6 引文斯高帕斯（Scopus）

摘要

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.

原文	英語
頁（從 - 到）	2096-2102
頁數	7
期刊	Environmental Toxicology
卷	37
發行號	8
DOIs	https://doi.org/10.1002/tox.23553
出版狀態	接受/付印 - 2022

ASJC Scopus subject areas

毒理學
管理、監督、政策法律
健康、毒理學和誘變

UN SDG

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10.1002/tox.23553

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Lin, C. Y., Lin, Y. C., Paul, C. R., Hsieh, D. J. Y., Day, C. H., Chen, R. J., Kuo, C. H., Ho, T. J., Shibu, M. A., Lai, C. H., Shih, T. C., Kuo, W. W., & Huang, C. Y. (認可的出版社/出版中). Isoliquiritigenin ameliorates advanced glycation end-products toxicity on renal proximal tubular epithelial cells. Environmental Toxicology, 37(8), 2096-2102. https://doi.org/10.1002/tox.23553

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title = "Isoliquiritigenin ameliorates advanced glycation end-products toxicity on renal proximal tubular epithelial cells",

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.",

keywords = "diabetic nephropathy, epithelial-myofibroblast transdifferentiation, fibrosis, radix Glycyrrhizae",

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

note = "Funding Information: The study was supported by grants received from China Medical University and Asia University, Taiwan (CMU107‐ASIA‐10). Publisher Copyright: {\textcopyright} 2022 Wiley Periodicals LLC.",

year = "2022",

doi = "10.1002/tox.23553",

language = "English",

volume = "37",

pages = "2096--2102",

journal = "Environmental Toxicology",

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AU - Lin, Chin Yi

AU - Lin, Yu Cheng

AU - Paul, Catherine Reena

AU - Hsieh, Dennis Jine Yuan

AU - Day, Cecilia Hsuan

AU - Chen, Ray Jade

AU - Kuo, Chia Hua

AU - Ho, Tsung Jung

AU - Shibu, Marthandam Asokan

AU - Lai, Chin Hu

AU - Shih, Tzu Ching

AU - Kuo, Wei Wen

AU - Huang, Chih Yang

PY - 2022

Y1 - 2022

N2 - 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.

AB - 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.

KW - diabetic nephropathy

KW - epithelial-myofibroblast transdifferentiation

KW - fibrosis

KW - radix Glycyrrhizae

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

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