Exendin-4 attenuates renal tubular injury by decreasing oxidative stress and inflammation in streptozotocin-induced diabetic mice.

Sancar-Bas S., Gezginci-Oktayoglu S., Bolkent Ş.

Growth factors (Chur, Switzerland), cilt.33, ss.419-29, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33
  • Basım Tarihi: 2015
  • Doi Numarası: 10.3109/08977194.2015.1125349
  • Dergi Adı: Growth factors (Chur, Switzerland)
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.419-29
  • Anahtar Kelimeler: Diabetic nephropathy, exendin-4, inflammation, oxidative stress, renal tubular injury, GLUCAGON-LIKE PEPTIDE-1, INTERCELLULAR-ADHESION MOLECULE-1, TUMOR-NECROSIS-FACTOR, GENE-EXPRESSION, RECEPTOR EXPRESSION, EPITHELIAL-CELLS, HIGH GLUCOSE, KAPPA-B, NEPHROPATHY, KIDNEY
  • İstanbul Üniversitesi Adresli: Evet

Özet

In this study, we aimed to research the restorative effects of exendin-4, a GLP-1 analog, on renal tubular injury in streptozotocin-induced diabetes model. BALB/c male mice were divided into four groups: non-diabetic, non-diabetic+exendin-4 (3g/kg), diabetic and diabetic+exendin-4. In our diabetic model, we observed renal injury mainly in tubular area rather than glomeruli and exendin-4 decreased tubular injury with its glucose lowering effect. Besides, PCNA positive tubular cells, activities of LDH and Na+-K+-ATPase were also significantly declined by the administration of exendin-4. Furthermore, exendin-4 attenuated the levels of ROS, MDA, 8-OHdG, proinflammatory cytokines (TNF-, IL-1), chemokine MCP-1, ICAM-1, and fibrosis-related molecules (transforming growth factor 1 and fibronectin). In consistent with reducing tubular injury, macrophage infiltration and both MCP-1 and ICAM-1 production in tubular cells were decreased. These results indicate that exendin-4 may decrease renal tubular injury seen in the beginning of diabetic nephropathy by decreasing ROS production and inflammation.