Aristolochic acid-induced accumulation of methylglyoxal and N                     ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy

Yi Chieh Li; Shin Han Tsai; Shih Ming Chen; Ya Min Chang; Tzu Chuan Huang; Yu Ping Huang; Chen Tien Chang; Jen Ai Lee

doi:10.1016/j.bbrc.2012.06.049

Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy

Yi Chieh Li, Shin Han Tsai, Shih Ming Chen, Ya Min Chang, Tzu Chuan Huang, Yu Ping Huang, Chen Tien Chang, Jen Ai Lee

研究成果: 雜誌貢獻 › 文章 › 同行評審

31 引文斯高帕斯（Scopus）

摘要

Aristolochic acid, found in the Aristolochia species, causes aristolochic acid nephropathy (AAN) and can develop into renal failure. Methylglyoxal (MGO) is a highly cytotoxic compound generated from the metabolic process of glucose or fatty acids. It binds to proteins and forms N ε-(carboxymethyl)lysine (CML), which contributes to aging and diabetes mellitus complications. However, no relevant literature explores the relationship of MGO and CML with AAN. By injecting AA (10mg/kg BW) into C3H/He mice for 5 consecutive days, we successfully developed an AAN model and observed tubular atrophy with decreased renal function. Creatinine clearance also decreased from 10.32±0.79ml/min/kg to 2.19±0.29ml/min/kg (p

原文	英語
頁（從 - 到）	832-837
頁數	6
期刊	Biochemical and Biophysical Research Communications
卷	423
發行號	4
DOIs	https://doi.org/10.1016/j.bbrc.2012.06.049
出版狀態	已發佈 - 七月 13 2012

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDG

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10.1016/j.bbrc.2012.06.049

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引用此

Li, Y. C., Tsai, S. H., Chen, S. M., Chang, Y. M., Huang, T. C., Huang, Y. P., Chang, C. T., & Lee, J. A. (2012). Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. Biochemical and Biophysical Research Communications, 423(4), 832-837. https://doi.org/10.1016/j.bbrc.2012.06.049

Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine : An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. / Li, Yi Chieh; Tsai, Shin Han ; Chen, Shih Ming; Chang, Ya Min; Huang, Tzu Chuan; Huang, Yu Ping; Chang, Chen Tien; Lee, Jen Ai.

於: Biochemical and Biophysical Research Communications, 卷 423, 編號 4, 13.07.2012, p. 832-837.

研究成果: 雜誌貢獻 › 文章 › 同行評審

Li, YC, Tsai, SH , Chen, SM, Chang, YM, Huang, TC, Huang, YP, Chang, CT & Lee, JA 2012, 'Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy', Biochemical and Biophysical Research Communications, 卷 423, 編號 4, 頁 832-837. https://doi.org/10.1016/j.bbrc.2012.06.049

Li YC, Tsai SH , Chen SM, Chang YM, Huang TC, Huang YP 等. Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. Biochemical and Biophysical Research Communications. 2012 7月 13;423(4):832-837. https://doi.org/10.1016/j.bbrc.2012.06.049

Li, Yi Chieh ; Tsai, Shin Han ; Chen, Shih Ming ; Chang, Ya Min ; Huang, Tzu Chuan ; Huang, Yu Ping ; Chang, Chen Tien ; Lee, Jen Ai. / Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine : An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. 於: Biochemical and Biophysical Research Communications. 2012 ; 卷 423, 編號 4. 頁 832-837.

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abstract = "Aristolochic acid, found in the Aristolochia species, causes aristolochic acid nephropathy (AAN) and can develop into renal failure. Methylglyoxal (MGO) is a highly cytotoxic compound generated from the metabolic process of glucose or fatty acids. It binds to proteins and forms N ε-(carboxymethyl)lysine (CML), which contributes to aging and diabetes mellitus complications. However, no relevant literature explores the relationship of MGO and CML with AAN. By injecting AA (10mg/kg BW) into C3H/He mice for 5 consecutive days, we successfully developed an AAN model and observed tubular atrophy with decreased renal function. Creatinine clearance also decreased from 10.32±0.79ml/min/kg to 2.19±0.29ml/min/kg (p",

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note = "Funding Information: The authors would like to thank Han, Chuan-Hsiao, and Chang, Chia-hao for their useful advice on experimental techniques. This study was financially supported by the Shuang-Ho Medical Center–Taipei Medical University Joint Research Program ( 99TMU-SHH-04-4 ).",

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AU - Huang, Yu Ping

AU - Chang, Chen Tien

AU - Lee, Jen Ai

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