Protective effect of rosmarinus officinalis extract on the nephrotoxicity caused by nickel chloride in wistar rats

Hichem Saker, Samira Boussekine, Salim Gasmi, Abdkarim Benkhedir, Yasmine Benali, Chawki Bensouici

Protective effect of rosmarinus officinalis extract on the nephrotoxicity caused by nickel chloride in wistar rats

Číslo: 6/2022/2023
Periodikum: Journal of Microbiology, Biotechnology and Food Sciences
DOI: 10.55251/jmbfs.9764

Klíčová slova: Oxidative stress, Nickel, Rosmarinus officinalis, Nephrotoxicity, Rats

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Anotace: Nickel is a common environmental pollutant inducing nephrotoxicity. Oxidative stress has been proposed as a possible mechanism involved in this toxicity. The present study aimed to elucidate the potential protective effect of methanolic extract of Rosmarinus officinalis (RO) against nephrotoxicity induced by Nickel Chloride (NiCl2). The antioxidant activity and the metal chelating power of the plant extract were evaluated. An in vivo study on 28 rats divided into equal four groups including the first group as the control; the second received 100 mg/kg bw of RO extract; the third was exposed to 10 mg/kg bw of NiCl2, and the last was treated with the combination of the extract and NiCl2 by gavage for 28 days. Oxidative stress parameters, biochemical biomarkers, and histopathological examination of the kidney were determined. Analysis of the results showed that the plant has significant antioxidant and metal-chelating power. In addition, exposure of rats to NiCl2 caused a disturbance of renal function (urea, creatinine, and uric acid). This exposure also induced a renal oxidative stress, which results in increased MDA level and GST activity a decrease in antioxidant status (CAT, GPx, and SOD activity), and alteration in tissue architecture of kidney was observed. Co-administration of RO (extract and NiCl2) restored most of the parameters cited above to values close to normal. Therefore, the present study revealed the ability of RO to bind to NiCl2 and protect kidney tissue from NiCl2-induced oxidative damage.