Nephroprotective effect of Apium graveolens L. against Cisplatin-induced nephrotoxicity

Abstract

Background Cisplatin is extensively used in treating cancers, and its primary side-effect is nephrotoxicity. It accumulates in proximal convoluted tubules where it promotes cellular damage by oxidative stress, apoptosis, and inflammation, etc. In Unani medicine, Tukhm-e - Karafs (Apium graveolens L.) (TK) is mentioned in the literature to manage various kidney ailments due to its diuretic and deobstruent activities. Objective To investigate the nephroprotective effects of powder of TK in Cisplatin-induced nephrotoxicity in an animal model and to validate the Unani claim of its nephroprotective action. Material and methods In curative protocol, cisplatin (5 mg/kg body weight i.p) was administered on day one and powder of TK (500 and 1000 mg/kg p.o.) from the sixth day onwards for ten days. TK (500 and 1000 mg/kg p.o.) was given for ten days and Cisplatin (5 mg/kg body weight i.p) on day 11 in the protective model. At the end of the study, all the animals were sacrificed, and renal biochemical parameters were determined. KIM-1 level was also investigated in the kidney homogenate in conjunction with histopathological inspection of kidney tissues. Results Significant increase in serum creatinine and BUN, presence of mononuclear cell infiltration, tubular dilation and vacuolation in renal histopathology, and increased KIM-1 level confirmed the nephrotoxicity due to Cisplatin. TK's administration protects the kidney as suggested by the changes in biochemical renal function, decreased level of KIM-1, and improvement in histopathological changes. Conclusion The result advocated that TK prevented renal injury and maintained normal renal function in both models. It may be due to improved clearance of Cisplatin from kidney tubules and reduction in reactive oxygen species (ROS) produced by the inflammatory response.

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Protective Effect of Gamma Aminobutyric Acid against Aggravation of Renal Injury Caused by High Salt Intake in Cisplatin-Induced Nephrotoxicity

“…It is widely accepted as a representative kidney disease model to investigate acute nephrotoxicity [ 27 , 28 ]. Numerous studies have verified that when an acute renal injury occurs, blood BUN, serum creatinine, and glomerular filtration rate are increased in cisplatin-exposed rodents [ 29 , 30 , 31 ]. Furthermore, it has been established that cisplatin can induce histological changes including mononuclear cell infiltration, hemorrhages, tubular dilation, and vacuolation in kidney tissues [ 30 , 32 ].…”

The Effect of Ashitaba (Angelica keiskei (Miq.) Koidz.)) Sap on the Total Cholesterol Levels of Cisplatin-Induced Wistar Rats

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