Abstract
BackgroundAcute kidney injury (AKI) is a serious clinical problem with high rate of mortality and morbidity. Currently used prophylactic and therapeutic strategies to address AKI are limited and warrant further studies. In the present study an attempt was made to investigate the effect of quinacrine, a phospholipase A2 inhibitor against glycerol induced AKI in rats.MethodsAdult female Wistar rats were divided in to five groups. After 24 h of water deprivation rats in groups 3, 4 and 5 received an intraperitoneal injection of quinacrine (3 mg/kg, 10 mg/kg and 30 mg/kg of body weight respectively). Thirty minutes after the first injection of quinacrine animals in groups 3, 4 and 5 received an intramuscular injection of 25% glycerol (10 ml/kg of body weight). The animals in group 2 received 25% glycerol (10 ml/kg of body weight) only whereas rats in group 1 served as control . The quinacrine administration was continued once daily for three days, on the fourth day animals were sacrificed, blood and kidney were collected for various biochemical and histopathological studies.ResultsGlycerol treatment produced significant renal structural abnormalities and functional impairment (increased urea and creatinine). Increase in myeloperoxidase (MPO) and malondialdehyde (MDA) clearly suggested the involvement of oxidative stress and neutrophilic activity following glycerol administration. Quinacrine dose dependently attenuated glycerol induced structural and functional changes in kidney.ConclusionThe reversal of glycerol induced AKI by quinacrine points towards a role of phospholipase A2 (PLA2) in the pathogenesis of renal injury. The result of this study suggests that quinacrine may offer an alternative mode of treatment for AKI.
Highlights
Acute kidney injury (AKI) is a serious clinical problem with high rate of mortality and morbidity
Effect of glycerol and quinacrine on blood urea nitrogen and serum creatinine The BUN and Serum creatinine (Scr). the two principal clusters of renal function biomarkers were recorded in this study
The level of serum BUN following low (46.1 ± 10.7 mg/dL, P < 0.05), medium (38.1 ± 3.5 mg/dL, P < 0.05), and high (33.0 ± 0.7 mg/dL, P < 0.01) dose treatment of quinacrine showed a significant attenuation of glycerol induced increase in BUN level (Fig. 1a)
Summary
Acute kidney injury (AKI) is a serious clinical problem with high rate of mortality and morbidity. In the present study an attempt was made to investigate the effect of quinacrine, a phospholipase A2 inhibitor against glycerol induced AKI in rats. Previously termed acute renal failure, is associated with increased mortality, prolonged hospital stay, and accelerated chronic kidney disease. The search for effective therapy to accelerate recovery and attempts to prevent AKI have attracted much attention. Some recent studies suggested that glycerol induced ischemic insult to the renal tissue may result in derangement of cellar phospholipid membranes, which may trigger a sequence of biochemical events leading to irreversible cell injury, presumably due to enhanced generation of oxygen derived free radicals and activation of tissue phospholipases [13, 14]
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