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Rosiglitazone Protects Against Cyclosporine‐Induced Pancreatic and Renal Injury in Rats
Author(s) -
Chung Byung Ha,
Li Can,
Sun Bo Kyung,
Lim Sun Woo,
Ahn Kyung Ohk,
Yang Ji Hun,
Choi Yoon Hee,
Yoon Kun Ho,
Sugawara Akira,
Ito Sadayoshi,
Kim Jin,
Yang Chul Woo
Publication year - 2005
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2005.00979.x
Subject(s) - medicine , rosiglitazone , endocrinology , fibrosis , kidney , pancreatic injury , renal function , diabetes mellitus , pancreas
Rosiglitazone (RGTZ) has protective effect against various types of injury. This study was performed to evaluate the effect of RGTZ on pancreatic and renal injury caused by cyclosporine (CsA). CsA (15 mg/kg) and RGTZ (3 mg/kg) were administered alone and together to the rats for 28 days. The effect of RGTZ on CsA‐induced pancreatic injury was evaluated by intraperitoneal glucose tolerance test (IPGTT), plasma insulin concentrations and pancreatic β‐cell morphology. The effect of RGTZ on CsA‐induced renal injury was evaluated by assessing renal function and pathology; mediators of inflammation and fibrosis such as angiotensin II (AngII), osteopontin (OPN) and transforming growth factor‐beta1 (TGF‐β1) and apoptotic cell death. Four weeks of CsA treatment caused diabetes, renal dysfunction, typical pathologic lesions (arteriolopathy, interstitial fibrosis and inflammatory cells infiltration) and apoptotic cell death. RGTZ treatment decreased blood glucose concentration, increased plasma insulin concentration and preserved pancreatic β islet mass. RGTZ treatment improved renal function and histopathology. Pro‐inflammatory and pro‐fibrotic molecules such as AngII, OPN and TGF‐β1, and apoptotic cell death also decreased with RGTZ treatment. These data suggest that RGTZ has a protective effect against CsA‐induced pancreatic and renal injury.