Abstract

Alhagi camelorum (AC) is an old plant with a significant therapeutic value throughout Africa, Asia, and Latin America. The overuse of cisplatin (Cis > 50 mg/m2) is associated with observed nephrotoxicity, ototoxicity, gastrotoxicity, myelosuppression, and allergic reactions. Remedial measures are needed for the protection of nephrotoxicity against cisplatin. Thus, we investigated the nephroprotective effects of AC plant extract to prevent cisplatin-induced nephrotoxicity in albino Wistar rats. The presence of polyphenols, phenolic compounds, tannins, and saponins was revealed during phytochemical investigation, and a significantly intense antioxidant activity was recorded. There were no toxicological symptoms in the treated rats, and no anatomical, physiological, or histological abnormalities were found compared to the control rats. The results of correcting cisplatin-induced nephrotoxicity revealed that the extract has a significant ability to treat kidney damage, with most parameters returning to normal after only three weeks of therapy. It is concluded that co-administration of cisplatin with AC extract showed exceptional nephroprotective effects at a dose of 600 mg/kg for Cis-induced nephrotoxicity.

Highlights

  • IntroductionNephrotoxicity is one of the most persistent kidney problems with an 8–15% lifetime risk in Europe, 2–5% in Asia, and 20% in the MiddleEast [1]

  • According to emerging evidence, nephrotoxicity is one of the most persistent kidney problems with an 8–15% lifetime risk in Europe, 2–5% in Asia, and 20% in the MiddleEast [1]

  • The results of different antioxidant assays showed that the concentration-dependent DPPH radical scavenging activity of the ethanol extract of A. camelorum was highest at 3000 mg/mL (96.07%), whereas the lowest (26.07%) was measured at 500 μg/mL

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Summary

Introduction

Nephrotoxicity is one of the most persistent kidney problems with an 8–15% lifetime risk in Europe, 2–5% in Asia, and 20% in the MiddleEast [1]. Kidneys account for 25% of the heat output and are naturally exposed to circulatory drugs and chemicals as central excretion bodies. These nephrotoxic drugs contribute to acute kidney failure and increased morbidity and death [3,4]. Because of their functions in glomerular concentrations, drug delivery, and metabolism, the epithelial cells of the renal proximal convoluted tubules (PCT) are a crucial target for nephrotoxicants [5]. Nephrotoxic agents usually damage the renal tubular epithelial cells either by reacting indirectly (through metabolites) or directly with membrane components and cellular macromolecules [6,7]

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