7-O-Galloyl-D-sedoheptulose ameliorates renal damage triggered by reactive oxygen species-sensitive pathway of inflammation and apoptosis

Journal of Pharmacy and Pharmacology

Volumn 64, Issue 12, 2012, Pages 1730-1740

  Park, Chan Hum ^a   Noh, Jeong Sook ^a   Tanaka, Takashi ^b   Yokozawa, Takako ^a  

^a UNIVERSITY OF TOYAMA   (Japan)

^b NAGASAKI UNIVERSITY   (Japan)

Author keywords

7 O galloyl d sedoheptulose; apoptosis; diabetic kidney; inflammation; oxidative stress

Indexed keywords

7 O GALLOYL DEXTRO SEDOHEPTULOSE; CORNUS OFFICINALIS EXTRACT; CYCLOOXYGENASE 2; CYTOCHROME C; GLUTATHIONE; GLUTATHIONE DISULFIDE; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INDUCIBLE NITRIC OXIDE SYNTHASE; NITRIC OXIDE SYNTHASE; PHENOL DERIVATIVE; PROTEIN BAX; PROTEIN BCL 2; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE 4; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE P22PHOX SUBUNIT; THIOBARBITURIC ACID REACTIVE SUBSTANCE; TRANSCRIPTION FACTOR RELA; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT ACTIVITY; APOPTOSIS; ARTICLE; CONTROLLED STUDY; CORNUS; CORNUS OFFICINALIS; DIABETIC NEPHROPATHY; DRUG DOSE COMPARISON; DRUG EFFICACY; DRUG STRUCTURE; DRUG TARGETING; HISTOPATHOLOGY; KIDNEY PARENCHYMA; LIPID PEROXIDATION; MALE; MOUSE; NEPHRITIS; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; OXIDATIVE STRESS; PROTEIN EXPRESSION; RENAL PROTECTION; SIGNAL TRANSDUCTION; TREATMENT DURATION;

ANIMALS; ANTI-INFLAMMATORY AGENTS; ANTIOXIDANTS; APOPTOSIS; APOPTOSIS REGULATORY PROTEINS; CORNUS; DIABETES MELLITUS, TYPE 2; DIABETIC NEPHROPATHIES; GLUTATHIONE; HEPTOSES; INFLAMMATION; INFLAMMATION MEDIATORS; KIDNEY; LIPID PEROXIDATION; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NADPH OXIDASE; OXIDATIVE STRESS; PHENOLS; PHYTOTHERAPY; PLANT EXTRACTS; REACTIVE OXYGEN SPECIES;

EID: 84869089892     PISSN: 00223573     EISSN: 20427158     Source Type: Journal    
DOI: 10.1111/j.2042-7158.2012.01559.x     Document Type: Article

References (40)

1. Baynes JW, Thorpe SR,. Role of oxidative stress in diabetic complications: a new perspective on an old paradigm. Diabetes 1999; 48: 1-9.
2. Forbes JM, et al,. Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes 2008; 57: 1446-1454.
3. Sedeek M, et al,. Critical role of Nox4-based NADPH oxidase in glucose-induced oxidative stress in the kidney: implications in type 2 diabetic nephropathy. Am J Physiol Renal Physiol 2010; 299: F1348-F1358.
4. Yamabe N, et al,. Beneficial effect of Corni Fructus, a constituent of Hachimi-jio-gan, on advanced glycation end-product-mediated renal injury in streptozotocin-treated diabetic rats. Biol Pharm Bull 2007; 30: 520-526.
5. Yamabe N, et al,. Identification of antidiabetic effect of iridoid glycosides and low molecular weight polyphenol fractions of Corni Fructus, a constituent of Hachimi-jio-gan, in streptozotocin-induced diabetic rats. Biol Pharm Bull 2007; 30: 1289-1296.
6. Yamabe N, et al,. 7-O-Galloyl-d-sedoheptulose is a novel therapeutic agent against oxidative stress and advanced glycation endproducts in the diabetic kidney. Biol Pharm Bull 2009; 32: 657-664.
7. Yokozawa T, et al,. Novel action of 7-O-galloyl-d-sedoheptulose isolated from Corni Fructus as a hypertriglyceridaemic agent. J Pharm Pharmacol 2009; 61: 653-661.
8. Park CH, et al,. Beneficial effect of 7-O-galloyl-d-sedoheptulose on oxidative stress and hepatic and renal changes in type 2 diabetic db/db mice. Eur J Pharmacol 2010; 640: 233-242.
9. Sharma K, et al,. Diabetic kidney disease in the db/db mouse. Am J Physiol 2003; 284: F1138-F1144.
10. Yokozawa T, et al,. Protective effects of morroniside isolated from Corni Fructus against renal damage in streptozotocin-induced diabetic rats. Biol Pharm Bull 2008; 31: 1422-1428.
11. Ali SF, et al,. Reactive oxygen species formation as a biomarker of methylmercury and trimethyltin neurotoxicity. Neurotoxicology 1992; 13: 637-648.
12. Naito C, Yamanaka T,. Lipid peroxides in atherosclerotic diseases. Nihon Ronen Igakkai Zasshi 1978; 15: 187-191.
13. Uchiyama M, Mihara M,. Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem 1978; 86: 271-278.
14. Hissin PJ, Hilf RA,. A fluorometric method for determination of oxidized and reduced glutathione in tissues. Anal Biochem 1976; 74: 214-226.
15. Itzhaki RF, Gill DMA,. A micro-biuret method for estimating proteins. Anal Biochem 1964; 9: 401-410.
16. Komatsu S,. Extraction of nuclear proteins. Methods Mol Biol 2007; 355: 73-77.
17. Lee HB, et al,. Reactive oxygen species-regulated signaling pathways in diabetic nephropathy. J Am Soc Nephrol 2003; 14: S241-S245.
18. Geiszt M, et al,. Identification of renox, an NAD(P)H oxidase in kidney. Proc Natl Acad Sci U S A 2000; 97: 8010-8014.
19. Nath KA, Norby SM,. Reactive oxygen species and acute renal failure. Am J Med 2000; 109: 665-678.
20. Shiose A, et al,. A novel superoxide-producing NAD(P)H oxidase in kidney. J Biol Chem 2001; 276: 1417-1423.
21. Griendling KK, et al,. NAD(P)H oxidase: role in cardiovascular biology and disease. Circ Res 2000; 86: 494-501.
22. Zalba G, et al,. Oxidative stress in arterial hypertension: role of NAD(P)H oxidase. Hypertension 2001; 38: 1395-1399.
23. Gill PS, Wilcox CS,. MADPH oxidases in the kidney. Antioxid Redox Signal 2006; 8: 1597-1607.
24. Babior BM, et al,. The neutrophil NADPH oxidase. Arch Biochem Biophys 2002; 397: 342-344.
25. phox, in the kidney of streptozotocin-induced diabetic rats and its reversibity by interventive insulin treatment. Diabetologia 2003; 46: 1428-1437.
26. Gorin Y, et al,. Nox4 NAD(P)H oxidase mediates hypertrophy and fibronectin expression in the diabetic kidney. J Biol Chem 2005; 280: 39616-39626.
27. Nishikawa T, et al,. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature 2000; 404: 787-790.
28. Kumar D, et al,. Evidence of apoptosis in human diabetic kidney. Mol Cell Biochem 2004; 259: 67-70.
29. Susztak K, et al,. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. Diabetes 2006; 55: 225-233.
30. Baeuerle PA, Henkel T,. Function and activation of NF-κB in the immune system. Annu Rev Immunol 1994; 12: 141-179.
31. Viedt C, et al,. The terminal complement complex C5b-9 stimulates interleukin-6 production in human smooth muscle cells through activation of transcription factors NF-κB and AP-1. FASEB J 2000; 14: 2370-2372.
32. Surh YJ, et al,. Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: down-regulation of COX-2 and iNOS through suppression of NF-κB activation. Mutat Res 2001; 480-481: 243-268.
33. Komhoff M, et al,. Localization of cyclooxygenase-1 and -2 in adult and fetal human kidney: implication for renal function. Am J Physiol 1997; 272: F460-F468.
34. Adegboyega PA, Ololade O,. Immunohistochemical expression of cyclooxygenase-2 in normal kidneys. Appl Immunohistochem Mol Morphol 2004; 12: 71-74.
35. Rangel EB, et al,. Expression of cyclooxygenases during renal allograft rejection. Transplant Proc 2004; 36: 838-839.
36. Rangel EB, et al,. Up-regulation of cyclooxygenase-2 during acute human renal allograft rejection. Clin Transplant 2005; 19: 543-550.
37. Cheng H, et al,. Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression. J Am Soc Nephrol 2011; 22: 1240-1251.
38. Tian B, et al,. Mechanisms of cytokine induced NO-mediated cardiac fibroblast apoptosis. Am J Physiol Heart Circ Physiol 2002; 283: H1958-H1967.
39. Corbett JA, et al,. Tyrosine kinase involvement in IL-1 beta-induced expression of iNOS by beta-cells purified from islets of Langerhans. Am J Physiol 1994; 267: C48-C54.
40. Medeiros R, et al,. Connecting TNF-alpha signaling pathways to iNOS expression in a mouse model of Alzheimer's disease: relevance for the behavioral and synaptic deficits induced by amyloid beta protein. J Neurosci 2007; 27: 5394-5404.