title: Autologous transplantation of adipose-derived mesenchymal stem cells             ameliorates streptozotocin-induced diabetic nephropathy in rats by inhibiting             oxidative stress, pro-inflammatory cytokines and the p38 MAPK signaling pathway.
abstract: Diabetic nephropathy is the leading cause of end-stage renal disease. The             aim of this study was to investigate the renoprotective effects of autologous             transplantation of adipose-derived mesenchymal stem cells (ADMSCs) and to delineate             its underlying mechanisms of action in diabetic nephropathy. Diabetes was induced             in adult male Sprague-Dawley rats by streptozotocin (STZ) injection. ADMSCs were             administered intravenously 4 weeks after STZ injection and metabolic indices and             renal structure were assessed (12 weeks). Markers of diabetes including blood             glucose, cholesterol, triglycerides, urea nitrogen and creatinine were measured.             Renal pathology, levels of oxidative stress and the expression of pro-inflammatory             cytokines and the MAPK signaling pathway members were also determined. Autologous             transplantation of ADMSCs significantly attenuated common metabolic disorder symptoms             associated with diabetes. Furthermore, ADMSC administration minimized pathological             alterations, reduced oxidative damage and suppressed the expression of pro-inflammatory             cytokines in the renal tissues of diabetic rats. ADMSC transplantation also decreased             the expression of p-p38, p-ERK and p-JNK, which are all important molecules of             the MAPK signaling pathway. In conclusion, we provide experimental evidence demonstrating             that autologous transplantation of ADMSCs can be used therapeutically to improve             metabolic disorder and relieve renal damage induced by diabetes, and that the             key mechanisms underlying the positive therapeutic impact of ADMSC treatment in             kidneys could be due to the suppression of inflammatory response and oxidative             stress.
authors.affiliation: Department of Anatomy, College of Basic Medical Sciences, China                     Medical University, Shenyang 110001, P.R. China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Fang
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Tian
authors.forename: Shuling
authors.initials: S
authors.lastname: Bai
authors.forename: Jun
authors.initials: J
authors.lastname: Fan
authors.forename: Weijian
authors.initials: W
authors.lastname: Hou
authors.forename: Hao
authors.initials: H
authors.lastname: Tong
authors.forename: Dehua
authors.initials: D
authors.lastname: Li
mesh_terms: D000273:Adipose Tissue / Q000166:cytology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001806:Blood Urea Nitrogen; D002784:Cholesterol / Q000097:blood; D003404:Creatinine / Q000097:blood; D016207:Cytokines / Q000037:antagonists & inhibitors* / Q000378:metabolism; D003928:Diabetic Nephropathies / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D007668:Kidney / Q000473:pathology; D020935:MAP Kinase Signaling System; D008297:Male; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D014182:Transplantation, Autologous; D014280:Triglycerides / Q000097:blood; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D014280:Triglycerides; D013311:Streptozocin; D002784:Cholesterol; D003404:Creatinine; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases