Role of Oxidative Stress, Apoptosis and Autophagy in Cadmium-induced Renal Injury in Rats: Renoprotective Effect of Ghrelin

Background: Kidney diseases are one of the most common disorders of the modern life. Cadmium (Cd)-induced kidney damage is a common cause of chronic renal failure. Several mechanisms have been postulated to explain the mechanisms underlying Cd induced renal injury such as oxidative stress, apoptosis and autophagy. The aim of the present study was to examine the effect of ghrelin(AG) on renal damage induced by Cd and possible mechanisms Methods: Thirty male Sprague Dawley rats were subdivided into 3 equal groups; Group I (control) the vehicle control, Group II (Cd) group in which rats were subjected to 5 mg Cd/Kg/d via gastric gavage for 4 weeks, Group III (AG) as group II but rats were treated with 3 nmol of ghrelin/animal per day via subcutaneously route for 4 weeks. By the end of experiment, serum levels of creatinine ,Na+ and K, the levels of lipid peroxidations marker (MDA) and antioxidants (GSH) in kidney tissues, kidney injury molecule-1 (Kim-1) in urine and the expression of caspase-3 and LC3 in kidney tissues were measured. Results: Cd administration caused significant increase in serum creatinine and k, urine KIM1 with significant increase in kidney tissues LC3, caspase 3 and MDA that was concomitant with a significant decrease in GSH in (p< 0.05). Administration of AG with Cd caused significant improvement in the studied parameters. Conclusion: we concluded that AG attenuates the renal injury induced by cadmium, which might be due to attenuation of apoptosis, oxidative stress and autophagic process in kidney tissues.