<p>Protective Effect of <em>Croton macrostachyus</em> (Euphorbiaceae) Stem Bark on Cyclophosphamide-Induced Nephrotoxicity in Rats</p>

Abstract

Background: Cyclophosphamide is an alkylating antineoplastic agent and its major limitation is injury to normal tissue, leading to multiple organ toxicity, including kidney, heart, liver and reproductive toxicity. Croton macrostachyus (Euphorbiaceae) has been used in Ethiopian traditional medicine to manage renal diseases. Objective: The present study aims to assess the protective effect of the stem bark extract and solvent fractions of Croton macrostachyus on cyclophosphamide-induced nephrotoxicity in rats. Methods: Nephrotoxicity was induced using cyclophosphamide 200 mg/kg i.p injection on the first day of the experiment. The negative control groups were administered with cyclophosphamide alone (200 mg/kg, i.p.). The crude extracts were administered at three dose levels (100, 200, and 400 mg/kg), while aqueous and ethyl acetate fractions were given at two dose levels (100 and 200 mg/kg). Excepting the normal control, all groups were subjected to cyclophosphamide toxicity on the first day. Results: Treatment with crude extract 100 mg/kg and ethyl acetate fraction significantly decreased kidney-to-body weight ratio (P < 0.001). In addition, treatment with Croton macrostachyus crude extract and solvent fractions significantly decreased serum blood urea nitrogen (BUN) level (P < 0.001). Treatment with 100 and 200 mg/kg of ethyl acetate fraction significantly decreased serum creatinine level. Histopathological results confirmed the protective effect of the crude extract and solvent fractions of Croton macrostachyus. Conclusion: Croton macrostachyus possesses nephroprotective activities and it could be a possible source of treatment for cyclophosphamide-induced nephrotoxicity.

Protective Effects of Shorea roxburghii Phenolic Extract on Nephrotoxicity Induced by Cyclophosphamide: Impact on Oxidative Stress, Biochemical and Histopathological Alterations

“…The results from this study indicated that CTX significantly altered kidney function parameters as portrayed by elevated serum BUN, uric acid and creatinine. These results corroborated with previous studies indicating CTX mediated increase in serum renal toxicity markers [9,17] …”

“…These results corroborated with previous studies indicating CTX mediated increase in serum renal toxicity markers. [9,17] Several studies have indicated that increased concentration of serum creatinine, BUN and uric acid are indices of kidney damage which has been attributed to filtering of these biomarkers into the blood systemic circulation. [6,18] These typical biochemical parameters of kidney damage were amplified and confirmed by renal histopathological alterations including interstitial haemorrhage, degeneration of the glomerulus and renal atrophy.…”

The protective effect of glycyrrhizin against chemotherapy-related toxicity in kidneys of rats: An experimental approach

“…It also protects against toxicity of different organs including kidney [25][26] , liver [27] , and hurt [28] . CP-induced nephrotoxicity in rats [25,[29][30] , and in mice [31][32][33] have been reported. In rats, tubular epithelial degeneration [34] collagen bundles around vessels, tubules and also in glomeruli [29] , inflammatory cells infiltration, tubular necrosis [30] and glomerular necrosis [25] have been reported in kidneys of CP given animals.…”

“…CP-induced nephrotoxicity in rats [25,[29][30] , and in mice [31][32][33] have been reported. In rats, tubular epithelial degeneration [34] collagen bundles around vessels, tubules and also in glomeruli [29] , inflammatory cells infiltration, tubular necrosis [30] and glomerular necrosis [25] have been reported in kidneys of CP given animals. In mice, degeneration [31][32][33] , swelling [31][32] necrosis and congestion [32] , casts formation and atrophy [33] in tubuli and thickened basal membrane, widened Bowman's space [33] , degeneration [31,33] , atrophy [33] in glomeruli, and also inflammatory cells infiltration in cortical and medullary area [32][33] have been evaluated in CP-induced renal damage.…”

Anti-inflammatory and anti-apoptotic potential of beta-glucan on chemotherapy-induced nephrotoxicity in rats

“…However, the therapeutic use of CP is restricted due to the side effects it produces, such as nephrotoxicity, cardiotoxicity, and hepatotoxicity [3]. Renal damage induced by CP includes apoptosis and necrosis of tubular epithelial cells [3], inflammation [4], fibrosis [5], and decreased lysosomal enzyme activity [6]. The toxic mechanism of CP is attributed to its main metabolites, phosphoramide mustard and acrolein, which cause an increase in free radicals [7].…”