15^th Annual European Pharma Congress

Biography

Biography: Parnia Mobasheran

Abstract

Aim: Ischemic/reperfusion injury is the common cause for acute kidney injury. The aim of the present study is to investigate the effect of 5HT_1B/1D agonist on the renal ischemic injury in rats.

Method: Ischemia/reperfusion injury was induced by a 45-minute occlusion of the bilateral renal pedicles and a 24-hour reperfusion. Our experimental groups consist of sham, control, and treatments that received three doses of sumatriptan (5, 10, 20 mg/kg). Nitric oxide kit, selective and non-selective inhibitor of nitric oxide synthase (NOS), aminoguanidine, and L-NAME were used to determine the role of Nitric oxide system. Superoxide dismutase (SOD) and malondialdehyde (MDA) of the tissue were measured to investigate the role of inflammation. Histopathological study of the kidney was performed too.

Result: Serum creatinine (Cr) and blood urea nitrogen (BUN) were measured after 24 hours of reperfusion. Sumatriptan in doses of 10, 20 mg/kg increased Cr and BUN significantly. There was a significant increase (P<0.05) of nitric oxide (NO) level in the treatment group compared with the level of the control group. Comparing to sumatriptan alone, the result of aminoguanidine administration showed a significant decrease (P<0.01) in BUN and (P<0.05) Cr. Besides, there was a significant increase (P<0.05) in BUN level, but not in Cr level when both L-NAME and sumatriptan administered within one hour. We also observed a reduction of SOD level (P<0.05) and increased serum level of MDA (P<0.001); furthermore, the histopathological result indicates kidney damage.

Conclusion: The study conducted showed an increase in kidney damage due to use of sumatriptan. We proved that NO plays a significant role in this injury. Also, decreased levels of creatinine and blood urea nitrogen in response to the aminoguanidine injection showed that inducible NO was involved in this injury.