(+)-Catechin ameliorates diabetic nephropathy by trapping methylglyoxal in type 2 diabetic mice

Molecular Nutrition and Food Research

Volumn 58, Issue 12, 2014, Pages 2249-2260

  Zhu, Dina ^a   Wang, Lei ^a   Zhou, Qile ^b   Yan, Shijun ^a,d   Li, Zhi ^a   Sheng, Jun ^c   Zhang, Wensheng ^a  

^a BEIJING NORMAL UNIVERSITY   (China)

^b PEKING UNIVERSITY HEALTH SCIENCE CENTER   (China)

^c YUNNAN AGRICULTURAL UNIVERSITY   (China)

^d UNIVERSITY OF KANSAS   (United States)

Author keywords

(+) Catechin; db db mice; Diabetic nephropathy; Inflammation; Methylglyoxal

Indexed keywords

MUS;

ADVANCED GLYCATION END PRODUCT; CATECHIN; INTERLEUKIN 1BETA; METHYLGLYOXAL; TRANSCRIPTION FACTOR RELA; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL; C57BL MOUSE; CELL LINE; DIABETES MELLITUS, EXPERIMENTAL; DIABETIC NEPHROPATHIES; DISEASE COURSE; DOWN REGULATION; GENETICS; HUMAN; MALE; METABOLISM; MOUSE; PHOSPHORYLATION;

ANIMALS; CATECHIN; CELL LINE; DIABETES MELLITUS, EXPERIMENTAL; DIABETIC NEPHROPATHIES; DISEASE PROGRESSION; DOWN-REGULATION; GLYCOSYLATION END PRODUCTS, ADVANCED; HUMANS; INTERLEUKIN-1BETA; MALE; MICE; MICE, INBRED C57BL; PHOSPHORYLATION; PYRUVALDEHYDE; TRANSCRIPTION FACTOR RELA; TUMOR NECROSIS FACTOR-ALPHA;

EID: 84912067572     PISSN: 16134125     EISSN: 16134133     Source Type: Journal    
DOI: 10.1002/mnfr.201400533     Document Type: Article

References (52)

1. Locatelli, F., Pozzoni, P., Del, V. L., Renal replacement therapy in patients with diabetes and end-stage renal disease. J. Am. Soc. Nephrol. 2004, 15(Suppl 1), S25-S29.
2. Satirapoj, B., Nephropathy in diabetes. Adv. Exp. Med. Biol. 2012, 771, 107-122.
3. Krochak, R. J., Baker, D. G., Radiation nephritis. Clinical manifestations and pathophysiologic mechanisms. Urology 1986, 27, 389-393.
4. Thornalley, P. J., Langborg, A., Minhas, H. S., Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose. Biochem. J. 1999, 344(Pt 1), 109-116.
5. Bohlender, J. M., Franke, S., Stein, G., Wolf, G., Advanced glycation end products and the kidney. Am. J. Physiol. Renal. Physiol. 2005, 289, F645-F659.
6. Thornalley, P. J., Dicarbonyl intermediates in the maillard reaction. Ann. N. Y. Acad. Sci. 2005, 1043, 111-117.
7. Wang, H., Meng, Q. H., Gordon, J. R., Khandwala, H. et al., Proinflammatory and proapoptotic effects of methylglyoxal on neutrophils from patients with type 2 diabetes mellitus. Clin. Biochem. 2007, 40, 1232-1239.
8. Lu, J., Randell, E., Han, Y., Adeli, K. et al., Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy. Clin. Biochem. 2011, 44, 307-311.
9. Suzuki, D., Miyata, T., Carbonyl stress in the pathogenesis of diabetic nephropathy. Intern. Med. 1999, 38, 309-314.
10. Dobler, D., Ahmed, N., Song, L., Eboigbodin, K. E. et al., Increased dicarbonyl metabolism in endothelial cells in hyperglycemia induces anoikis and impairs angiogenesis by RGD and GFOGER motif modification. Diabetes 2006, 55, 1961-1969.
11. Falk, R. J., Scheinman, J. I., Mauer, S. M., Michael, A. F., Polyantigenic expansion of basement membrane constituents in diabetic nephropathy. Diabetes 1983, 32(Suppl 2), 34-39.
12. Dronavalli, S., Duka, I., Bakris, G. L., The pathogenesis of diabetic nephropathy. Nat. Clin. Pract. Endocrinol. Metab. 2008, 4, 444-452.
13. Semba, R. D., Nicklett, E. J., Ferrucci, L., Does accumulation of advanced glycation end products contribute to the aging phenotype? J. Gerontol. A Biol. Sci. Med. Sci. 2010, 65, 963-975.
14. Horie, K., Miyata, T., Maeda, K., Miyata, S. et al., Immunohistochemical colocalization of glycoxidation products and lipid peroxidation products in diabetic renal glomerular lesions. Implication for glycoxidative stress in the pathogenesis of diabetic nephropathy. J. Clin. Invest. 1997, 100, 2995-3004.
15. Ramasamy, R., Yan, S. F., Schmidt, A. M., Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications. Ann. N. Y. Acad. Sci. 2011, 1243, 88-102.
16. Schmidt, A. M., Yan, S. D., Yan, S. F., Stern, D. M., The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. J. Clin. Invest. 2001, 108, 949-955.
17. Aljada, A., Friedman, J., Ghanim, H., Mohanty, P. et al., Glucose ingestion induces an increase in intranuclear nuclear factor kappaB, a fall in cellular inhibitor kappaB, and an increase in tumor necrosis factor alpha messenger RNA by mononuclear cells in healthy human subjects. Metabolism 2006, 55, 1177-1185.
18. Sousa, M. M., Yan, S. D., Stern, D., Saraiva, M. J., Interaction of the receptor for advanced glycation end products (RAGE) with transthyretin triggers nuclear transcription factor kB (NF-kB) activation. Lab. Invest. 2000, 80, 1101-1110.
19. Wu, C. H., Yeh, C. T., Shih, P. H., Yen, G. C., Dietary phenolic acids attenuate multiple stages of protein glycation and high-glucose-stimulated proinflammatory IL-1beta activation by interfering with chromatin remodeling and transcription in monocytes. Mol. Nutr. Food Res. 2010, 54(Suppl 2), S127-S140.
20. Wu, C. C., Chen, J. S., Lu, K. C., Chen, C. C. et al., Aberrant cytokines/chemokines production correlate with proteinuria in patients with overt diabetic nephropathy. Clin. Chim. Acta 2010, 411, 700-704.
21. Goldberg, R. B., Cytokine and cytokine-like inflammation markers, endothelial dysfunction, and imbalanced coagulation in development of diabetes and its complications. J. Clin. Endocrinol. Metab. 2009, 94, 3171-3182.
22. Alexandraki, K., Piperi, C., Kalofoutis, C., Singh, J. et al., Inflammatory process in type 2 diabetes: the role of cytokines. Ann. N. Y. Acad. Sci. 2006, 1084, 89-117.
23. Harada, M., Kan, Y., Naoki, H., Fukui, Y. et al., Identification of the major antioxidative metabolites in biological fluids of the rat with ingested (+)-catechin and (-)-epicatechin. Biosci. Biotechnol. Biochem. 1999, 63, 973-977.
24. Bell, J. R., Donovan, J. L., Wong, R., Waterhouse, A. L. et al., (+)-Catechin in human plasma after ingestion of a single serving of reconstituted red wine. Am. J. Clin. Nutr. 2000, 71, 103-108.
25. Rhee, S. J., Kim, M. J., Kwag, O. G., Effects of green tea catechin on prostaglandin synthesis of renal glomerular and renal dysfunction in streptozotocin-induced diabetic rats. Asia Pac. J. Clin. Nutr. 2002, 11, 232-236.
26. Chander, V., Singh, D., Chopra, K., Catechin, a natural antioxidant protects against rhabdomyolysis-induced myoglobinuric acute renal failure. Pharmacol. Res. 2003, 48, 503-509.
27. Anjaneyulu, M., Tirkey, N., Chopra, K., Attenuation of cyclosporine-induced renal dysfunction by catechin: possible antioxidant mechanism. Ren. Fail. 2003, 25, 691-707.
28. Choi, J. H., Chai, Y. M., Joo, G. J., Rhee, I. K. et al., Effects of green tea catechin on polymorphonuclear leukocyte 5'-lipoxygenase activity, leukotriene B4 synthesis, and renal damage in diabetic rats. Ann. Nutr. Metab. 2004, 48, 151-155.
29. Suzuki, J., Ogawa, M., Izawa, A., Sagesaka, Y. M. et al., Dietary consumption of green tea catechins attenuate hyperlipidaemia-induced atherosclerosis and systemic organ damage in mice. Acta Cardiol. 2005, 60, 271-276.
30. Abd, E. T., Mohamed, R. H., Pasha, H. F., Abdel-Aziz, H. R., Catechin protects against oxidative stress and inflammatory-mediated cardiotoxicity in adriamycin-treated rats. Clin. Exp. Med. 2012, 12, 233-240.
31. Chennasamudram, S. P., Kudugunti, S., Boreddy, P. R., Moridani, M. Y. et al., Renoprotective effects of (+)-catechin in streptozotocin-induced diabetic rat model. Nutr. Res. 2012, 32, 347-356.
32. Waltner-Law, M. E., Wang, X. L., Law, B. K., Hall, R. K. et al., Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J. Biol. Chem. 2002, 277, 34933-34940.
33. Fudouji, R., Tanaka, T., Taguri, T., Matsuo, Y. et al., Coupling reactions of catechins with natural aldehydes and allyl alcohols and radical scavenging activities of the triglyceride-soluble products. J. Agric. Food Chem. 2009, 57, 6417-6424.
34. Sang, S., Shao, X., Bai, N., Lo, C. Y. et al., Tea polyphenol (-)-epigallocatechin-3-gallate: a new trapping agent of reactive dicarbonyl species. Chem. Res. Toxicol. 2007, 20, 1862-1870.
35. Totlani, V. M., Peterson, D. G., Epicatechin carbonyl-trapping reactions in aqueous maillard systems: identification and structural elucidation. J. Agric. Food Chem. 2006, 54, 7311-7318.
36. Lo, C. Y., Li, S., Tan, D., Pan, M. H. et al., Trapping reactions of reactive carbonyl species with tea polyphenols in simulated physiological conditions. Mol. Nutr. Food Res. 2006, 50, 1118-1128.
37. Kodama, H., Fujita, M., Yamaguchi, I., Development of hyperglycaemia and insulin resistance in conscious genetically diabetic (C57BL/KsJ-db/db) mice. Diabetologia 1994, 37, 739-744.
38. Sharma, K., McCue, P., Dunn, S. R., Diabetic kidney disease in the db/db mouse. Am. J. Physiol. Renal. Physiol. 2003, 284, F1138-F1144.
39. Yan, S. J., Wang, L., Li, Z., Zhu, D. N. et al., Inhibition of advanced glycation end product formation by Pu-erh tea ameliorates progression of experimental diabetic nephropathy. J. Agric. Food Chem. 2012, 60, 4102-4110.
40. Ruggiero-Lopez, D., Lecomte, M., Moinet, G., Patereau, G. et al., Reaction of metformin with dicarbonyl compounds. Possible implication in the inhibition of advanced glycation end product formation. Biochem. Pharmacol. 1999, 58, 1765-1773.
41. Beisswenger, P. J., Howell, S. K., Touchette, A. D., Lal, S. et al., Metformin reduces systemic methylglyoxal levels in type 2 diabetes. Diabetes 1999, 48, 198-202.
42. MacLean, M. J., Ness, L. S., Ferguson, G. P., Booth, I. R., The role of glyoxalase I in the detoxification of methylglyoxal and in the activation of the KefB K+ efflux system in Escherichia coli. Mol. Microbiol. 1998, 27, 563-571.
43. Thornalley, P. J., Glutathione-dependent detoxification of alpha-oxoaldehydes by the glyoxalase system: involvement in disease mechanisms and antiproliferative activity of glyoxalase I inhibitors. Chem. Biol. Interact. 1998, 111-112, 137-151.
44. Myint, K. M., Yamamoto, Y., Doi, T., Kato, I. et al., RAGE control of diabetic nephropathy in a mouse model: effects of RAGE gene disruption and administration of low-molecular weight heparin. Diabetes 2006, 55, 2510-2522.
45. Voziyan, P. A., Metz, T. O., Baynes, J. W., Hudson, B. G., A post-Amadori inhibitor pyridoxamine also inhibits chemical modification of proteins by scavenging carbonyl intermediates of carbohydrate and lipid degradation. J. Biol. Chem. 2002, 277, 3397-3403.
46. Nascimento, M. M., Suliman, M. E., Murayama, Y., Nihi, M. et al., Effect of high-dose thiamine and pyridoxine on advanced glycation end products and other oxidative stress markers in hemodialysis patients: a randomized placebo-controlled study. J. Ren. Nutr. 2006, 16, 119-124.
47. Freedman, B. I., Wuerth, J. P., Cartwright, K., Bain, R. P. et al., Design and baseline characteristics for the aminoguanidine Clinical Trial in Overt Type 2 Diabetic Nephropathy (ACTION II). Control Clin. Trials 1999, 20, 493-510.
48. Perrone, J., Phillips, C., Gaieski, D., Occult metformin toxicity in three patients with profound lactic acidosis. J. Emerg. Med. 2011, 40, 271-275.
49. Kanasaki, K., Taduri, G., Koya, D., Diabetic nephropathy: the role of inflammation in fibroblast activation and kidney fibrosis. Front Endocrinol. 2013, 4, 1-15.
50. Fornoni, A., Ijaz, A., Tejada, T., Lenz, O., Role of inflammation in diabetic nephropathy. Curr. Diabetes Rev. 2008, 4, 10-17.
51. Berlanga, J., Cibrian, D., Guillen, I., Freyre, F. et al., Methylglyoxal administration induces diabetes-like microvascular changes and perturbs the healing process of cutaneous wounds. Clin. Sci. 2005, 109, 83-95.
52. Yamawaki, H., Saito, K., Okada, M., Hara, Y., Methylglyoxal mediates vascular inflammation via JNK and p38 in human endothelial cells. Am. J. Physiol. Cell. Physiol. 2008, 295, C1510-C1517.