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Back‐regulation of six oxidative stress proteins with grape seed proanthocyanidin extracts in rat diabetic nephropathy
Author(s) -
Li BaoYing,
Cheng Mei,
Gao HaiQing,
Ma YaBing,
Xu Ling,
Li XianHua,
Li XiaoLi,
You BeiAn
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21658
Subject(s) - glycation , diabetic nephropathy , oxidative stress , glycated hemoglobin , streptozotocin , kidney , medicine , diabetes mellitus , endocrinology , advanced glycation end product , pharmacology , nephropathy , chemistry , type 2 diabetes
Diabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients. To prevent the development of this disease and to improve advanced kidney injury, effective therapies directed toward the key molecular target are required. Grape seed proanthocyanidin extracts (GSPE) have been reported to be effective in treating DN, while little is known about the functional protein changes. In this study, we used streptozotocin (STZ) to induce diabetic rats. GSPE (250 mg/kg body weight/day) were administrated to diabetic rats for 24 weeks. Serum glucose, glycated hemoglobin, and advanced glycation end products were determined. Consequently, 2‐D difference gel electrophoresis and mass spectrometry were used to investigate kidney protein profiles among the control, untreated and GSPE treated diabetic rats. Twenty‐five proteins were found either up‐regulated or down‐regulated in the kidneys of untreated diabetic rats. Only nine proteins in the kidneys of diabetic rats were found to be back‐regulated to normal levels after GSPE therapy. These back‐regulated proteins are involved in oxidative stress, glycosylation damage, and amino acids metabolism. Our findings might help to better understanding of the mechanism of DN, and provide novel targets for estimating the effects of GSPE therapy. J. Cell. Biochem. 104: 668–679, 2008. © 2008 Wiley‐Liss, Inc.