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Am. J. Biomed. Sci. 2016, 8(2), 160-168; doi: 10.5099/aj160200160
Received: 28 March 2016; | Revised: 05 May 2016; | Accepted: 16 May 2016


Insulin Like Growth Factor -1(IGF-1) Promotes Angiogenesis and Reverses Ischemia Reperfusion Induced Acute Kidney Injury in Rats: Role of VEGF and TGF-β1


Mona M. Allam

M.D. Medical physiology, Department of Physiology, Benha Faculty of Medicine, Benha University, Egypt.

Corresponding Author

Mona M. Allam

Department of Physiology

Benha Faculty of Medicine (http://www.fmed.bu.edu.eg/)

Benha, Qualubia


Tel: 002 01005413002

Email: monamaher8011@yahoo.com



Previous studies highlighted the effect of administering insulin-like growth factor I (IGF-I) in a model of ischemic acute kidney injury (AKI) in rats. We studied the effect of IGF-1 treatment on ischemia reperfusion induced AKI in rats focusing on angiogenesis as a potential mechanism underlying the effect of IGF-1. AKI was induced by nephrectomy of the left kidney while the right one's pedicle was clamped for 45 min then the clamp was removed to start reperfusion. Compared to AKI rats, rats administered IGF-I (100 µg/day) for 7 days post occlusion had significantly lower serum creatinine, blood urea nitrogen (BUN) and Aspartate Aminotransferase (AST) levels. Serum creatinine and BUN were used as indicators of impaired renal function, while serum concentration of AST was measured as an indicator of renal injury. Examining the levels of vascular endothelial growth factor (VEGF) and transforming growth factor β1 (TGF- β1) in the renal tissue revealed higher levels in the I-R+IGF-1 group compared to I-R group. Histopathological examination of the renal tissue in the IGF-1treated group showed an obvious angiogenic reaction occurred as a result of IGF-1 treatment. Neovascularization by such angiogenic agents may explain the action of IGF-1 during AKI. Overall, the current results provide evidence that the effect of IGF-1 on ischemia-reperfusion AKI involves induction of angiogenesis.

Keywords: Insulin like growth factor -1, Ischemia reperfusion, angiogenesis, VEGF, TGF β1.

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