Diphlorethohydroxycarmalol Attenuates Methylglyoxal-Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

被引：28
作者：
Cha, Seon-Heui [1 ,2 ,3 ]
Hwang, Yongha [1 ,2 ]
Heo, Soo-Jin [4 ]
Jun, Hee-Sook [1 ,2 ,3 ]
机构：
[1] Gachon Univ, Coll Pharm, Incheon 21936, South Korea
[2] Gachon Univ, Lee Gil Ya Canc & Diabet Inst, Incheon 21936, South Korea
[3] Gachon Gil Med Ctr, Gachon Med & Convergence Inst, Incheon 21565, South Korea
[4] KIOST, Jeju Int Marine Sci Ctr Res & Educ, Jeju 63349, South Korea
来源：
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY | 2018年 / 2018卷
基金：
新加坡国家研究基金会;
关键词：
ISHIGE-OKAMURAE; NATURAL-PRODUCTS; GLYOXALASE; NRF2; ANTIOXIDANT; HYPERGLYCEMIA; POLYPHENOLS; MECHANISMS; DISEASE; PATHOGENESIS;
D O I：
10.1155/2018/3654095
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Diabetic nephropathy is the leading cause of end-stage renal disease in patients with diabetes mellitus. Oxidative stress has been shown to play an important role in pathogeneses of renal damage in diabetic patients. Here, we investigated the protective effect of diphlorethohydroxycarmalol (DPHC), which is a polyphenol isolated from an edible seaweed, Ishige okamurae, on methylglyoxal-induced oxidative stress in HEK cells, a human embryonic kidney cell line. DPHC treatment inhibited methylglyoxal-(MGO-) induced cytotoxicity and ROS production. DPHC activated the Nrf2 transcription factor and increased the mRNA expression of antioxidant and detoxification enzymes, consequently reducing MGO-induced advanced glycation end product formation. In addition, DPHC increased glyoxalase-1 mRNA expression and attenuated MGO-induced advanced glycation end product formation in HEK cells. These results suggest that DPHC possesses a protective activity against MGO-induced cytotoxicity in human kidney cells by preventing oxidative stress and advanced glycation end product formation. Therefore, it could be used as a potential therapeutic agent for the prevention of diabetic nephropathy.
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页数：14
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共 69 条
[1]   Advanced glycation endproducts - role in pathology of diabetic complications [J].
Ahmed, N .
DIABETES RESEARCH AND CLINICAL PRACTICE, 2005, 67 (01) :3-21
[2]   Methylglyoxal and Advanced Glycation End products: Insight of the regulatory machinery affecting the myogenic program and of its modulation by natural compounds [J].
Baig, Mohammad Hassan ;
Jan, Arif Tasleem ;
Rabbani, Gulam ;
Ahmad, Khurshid ;
Ashraf, Jalaluddin M. ;
Kim, Taeyeon ;
Min, Han Sol ;
Lee, Yong Ho ;
Cho, Won-Kyung ;
Ma, Jin Yeul ;
Lee, Eun Ju ;
Choi, Inho .
SCIENTIFIC REPORTS, 2017, 7
[3]   Methylglyoxal in diabetes: link to treatment, glycaemic control and biomarkers of complications [J].
Beisswenger, Paul J. .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2014, 42 :450-456
[4]   Glucose and reactive oxygen species [J].
Bonnefont-Rousselot, D .
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE, 2002, 5 (05) :561-568
[5]   Overexpression of Glyoxalase-I Reduces Hyperglycemia-induced Levels of Advanced Glycation End Products and Oxidative Stress in Diabetic Rats [J].
Brouwers, Olaf ;
Niessen, Petra M. ;
Ferreira, Isabel ;
Miyata, Toshio ;
Scheffer, Peter G. ;
Teerlink, Tom ;
Schrauwen, Patrick ;
Brownlee, Michael ;
Stehouwer, Coen D. ;
Schalkwijk, Casper G. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (02) :1374-1380
[6]   Advanced glycation end-products and the kidney [J].
Busch, Martin ;
Franke, Sybille ;
Ruester, Christiane ;
Wolf, Gunter .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 2010, 40 (08) :742-755
[7]   Advanced glycation end-products produced systemically and by macrophages: A common contributor to inflammation and degenerative diseases [J].
Byun, Kyunghee ;
Yoo, YongCheol ;
Son, Myeongjoo ;
Lee, Jaesuk ;
Jeong, Goo-Bo ;
Park, Young Mok ;
Salekdeh, Ghasem Hosseini ;
Lee, Bonghee .
PHARMACOLOGY & THERAPEUTICS, 2017, 177 :44-55
[8]   Hydrogen Sulfide Mediates Cardioprotection Through Nrf2 Signaling [J].
Calvert, John W. ;
Jha, Saurabh ;
Gundewar, Susheel ;
Elrod, John W. ;
Ramachandran, Arun ;
Pattillo, Christopher B. ;
Kevil, Christopher G. ;
Lefer, David J. .
CIRCULATION RESEARCH, 2009, 105 (04) :365-U105
[9]   Low-molecular-weight chitosan scavenges methylglyoxal and Nε-(carboxyethyl)lysine, the major factors contributing to the pathogenesis of nephropathy [J].
Chou, Chu-Kuang ;
Chen, Shih-Ming ;
Li, Yi-Chieh ;
Huang, Tzu-Chuan ;
Lee, Jen-Ai .
SPRINGERPLUS, 2015, 4
[10]   Nrf2 Activators as Attractive Therapeutics or Diabetic Nephropathy [J].
de Haan, Judy B. .
DIABETES, 2011, 60 (11) :2683-2684
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