Nephroprotective Potential Effects of Ghrelin in Renal Ischemia-Reperfusion Injury in Rat

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Authors: Teba Jasim Mohammed, Israa Al-Yasiri, Abdullah Jasim, Ali A. Ahmed, and Najah R. Hadi
Published in: World Heart Journal, Volume 9 Issue 4 (2017)
Page Range: 293-301
ISSN: 1556-4002

ISBN: N/A Categories: ,

Table of Contents

ABSTRACT

Background. Renal injury from the impairment of blood flow to the kidney is due to ischemia / reperfusion (I/R) as in surgical procedure, as the kidney remains hypoperfused for some time. This is observed during kidney transplantation, vascular surgery of the aorta and renal arteries, and partial nephrectomy. Ghrelin is an orexigenic growth hormone secretagogue derived mainly from ghrelinergic cells in the gastro-intestinal tract (GIT). It plays an important physiological role in regulating energy homeostasis and appetite stimulation. In this study, we aimed to assess the ability of ghrelin to exert potential protective effects on the kidney I/R and subsequent kidney dysfunctions in the rat through inhibition of oxidative stress and apoptosis and modulation of inflammation.
Materials and Methods. Twenty-eight rats were used in this experiment. Ischemia/reperfusion (I/R) was induced in a rat model by unilateral renal artery clamping for 30 minutes and reperfusion for 3 hours. Ghrelin (40 µg/kg/rat) or vehicle was injected via intra-peritoneal (i.p.) route twice, once 30 minutes before induced ischemia and then immediately at the time of reperfusion. Ghrelin administration could exert a protective role on the kidney against injury by significantly reducing serum and tissue concentrations of malondialdehyde (MDA), caspase-3 and high mobility group box 1 protein (HMGB1), reducing serum concentrations of urea and creatinine, and reducing the severity of renal damage.
Conclusions. We conclude that ghrelin has renoprotective effects via inhibition of markers of oxidative stress and apoptosis along with modulation of inflammation.

Keywords: ghrelin, renal ischemia reperfusion injury, MDA, caspase-3.