Celery Ethanol Extract Prevents Renal Ischemia-Reperfusion Injury via Increasing Nitrite Oxide and Superoxide Dismutase

Abstract

Background: Acute kidney injury (AKI) is one of the health problems. Kidney ischemia-reperfusion injury (IRI) contributes to pathological conditions of AKI. An imbalance between renal vasoconstriction and vasodilatation mediators was played a role in IRI and its chronic complications. Stress oxidative and inflammation were major pathomechanism of IRI. Administration of celery ethanol extract is one of the efforts to prevent kidney damage caused by IRI. This study aimed to investigate the time effect of celery ethanol extract administration on inhibition of kidney IRI. Methods: Twenty male Sprague Dawley rats with a weight range of 190-210 g were selected for the study. The rats were divided into five groups randomly: sham operation (SO, n=4) group, IRI group (ischemia-reperfusion injury, n=4), IRI+S7 (celery ethanol extract 1000 mg/kg BW 7 days orally+ischemia-reperfusion injury, n=4), IRI+S14 (celery ethanol extract 1000 mg/kg BW 14 days orally+ischemia-reperfusion injury, n=4), IRI+S28 (celery ethanol extract 1000 mg/kg BW 28 days orally+ischemia-reperfusion injury, n=4). Serum samples were collected for creatinine serum, NO, SOD, and TNF-α measurement. mRNA expression of ET-1 and ETAR was quantified using reverse transcriptase-PCR. Result: Serum creatinine, NO, and SOD level in rats with celery ethanol extract 1000 mg/kg BW for 7 and 14 days administration before IRI induction lower than IRI group (p<0.05) and increase in 28 days administration. Meanwhile, the TNF-α level, ET-1, and ETAR gen expression lower than the IRI group but not significantly different (p>0.05). Conclusion: Administration of celery ethanol extract 1000 mg/kg BW for 7 days and 14 days prevents renal ischemia-reperfusion injury via increasing NO and SOD. Administration more than 28 days is not recommended.