An investigation on the effects of the calpain inhibitor AK295 on caspase 3 in renal ischemia reperfusion damage in rats

Calpains (Calcium activated proteases) are responsible for degradation of the cytoskeleton of the cells that are damaged irreparably. Calpains also have additional tasks such as facilitating the repair in forming the cytoskeleton and in sublethal axonal membrane damages. Calpains may take on common tasks with caspases in the cases such as necrosis and apoptosis that result in cell death. In the experimental studies done in recent years, it has been indicated by DNA fragmentation analyses that the calpain inhibitors slow down or stop apoptosis in the spinal cord trauma models in rats. Purpose of this study was to invastigate the effect of AK295, which is a calpain inhibitor, on caspase-3 enzyme via an experimental kidney ischemia-reperfusion model generated on rats.28 male Wistar Albino rats were divided into 4 randomgroups (n=7). These 4 groups were Group I (Control Group), Group II (Ischemia-reperfusion group), Group III (Ischemia-reperfusion + AK295 group), and Group IV (Ischemia-reperfusion + DMSO group). Right kidney nephrectomy under anesthesia of xylazine (5 mg/kg) and ketamine (75 mg/kg) was performed to the rats except for Group I. The rats under reversible general anesthesia underwent 30-minute total ischemia. At the end of the test, blood samples (5 cc) and kidney tissues were taken from all the groups rapidly. Caspase 3 enzyme activity was detected in the kidney tissues by Western-Blot technique. Serum creatine and urea values, amount of kidney malondialdehyde, and changes in the cellular antioxidant enzymes superoxide dismutase and catalase were also analyzed.As a result of the study, it was found that the calpain inhibitor AK295 partially inhibited apoptosis in kidney damage by ischemia-reperfusion, and had a protective effect against kidney damage.