The Effect of Insulin Treatment on Rac1 Expression in Diabetic Kidney

GÜMÜŞTEKİN M., CİLAKER MIÇILI S., ARICI M. A., KARAMAN M., GÜNELİ M. E., Tekmen I.

RENAL FAILURE, cilt.35, sa.3, ss.396-402, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 35 Sayı: 3
  • Basım Tarihi: 2013
  • Doi Numarası: 10.3109/0886022x.2013.764256
  • Dergi Adı: RENAL FAILURE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.396-402
  • Anahtar Kelimeler: apoptosis, caspase-3, diabetic nephropathy, insulin, Rac1, TUBULAR EPITHELIAL-CELLS, NADPH OXIDASE, OXIDATIVE STRESS, APOPTOSIS, MELATONIN, NEPHROPATHY, PROTECTS, GLUCOSE, GTPASE, DAMAGE
  • Dokuz Eylül Üniversitesi Adresli: Evet

Özet

This study was designed to evaluate the renoprotective effect of insulin on diabetic nephropathy through Rac1 inhibition. Twenty Wistar rats were divided into three groups: control (C), diabetic (D), and insulin-treated diabetic (D + I). Diabetes was induced by a single streptozotocin (STZ) injection (45 mg/kg i.p.) in adult male rats. Diabetic animals were treated subcutaneously with insulin (6 U/kg), or saline once a day for 8 weeks. Age-matched control rats received only saline. The kidney tissue samples were analyzed by immunohistochemical staining for Rac1 and cleaved caspase-3 expressions and using the TUNEL method for determining apoptotic cells. Diabetes increased the number of TUNEL (+) cells and cleaved caspase-3 and Rac1 expression levels in kidney. Administration of insulin for 8 weeks reduced Rac1 expression and ameliorated histopathological changes in kidney of STZ-induced diabetes model. These results may suggest that the renoprotective effect of insulin at least partly results from inhibition of Rac1 overexpression.