Flavonoids of Phoenix dactylifera L. ameliorates mercury-toxicity on the kidney of Wistar rats. A biochemical, morphological and molecular approach

Abstract

IntroductionOne of the primary target organs of mercury toxicity is the kidney. Inorganic mercury such as mercuric chloride (HgCl2) significantly damages the kidney. Phoenix dactylifera has been documented to possess several pharmacological activities. In traditional Chinese medicine, Phoenix dactylifera has been used to replenish energy during weakness, temper the harshness of other herbs, and treat a lot of ailments. This study evaluated the protective effects of the n-butanol fraction of Phoenix dactylifera L. (BFPD) on mercury-triggered kidney toxicity in Wistar rats. Method25 male Wistar rats were divided into 5 groups containing 5 rats each. Group I was the control and was administered 2 ml/kg of distilled water; group II was administered 5 mg/kg of HgCl2; group III was pretreated with 500 mg/kg of BFPD + 5 mg/kg of HgCl2; group IV was pretreated with 1000 mg/kg of BFPD + 5 mg/kg of HgCl2, while group V was pretreated with 100 mg/kg of silymarin + 5 mg/kg of HgCl2. orally for 2 weeks. The rats were euthanized and blood samples were collected for biochemical studies (kidney serum proteins (urea and creatinine), and oxidative stress biomarker, Glutathione peroxidase (GPx). Kidney samples were collected for immunohistochemical, stereological and molecular studies. ResultsThe results revealed that oxidative stress was induced in the rats exposed to HgCl2 evident by the altered levels of Urea, Creatinine, and GPx in comparison to the control. However, BFPD treatment restored these changes. GPx activity decreased (p <0.05) in the HgCl2-treated group in comparison to the control and BFPD-treated groups. The HgCl2 treated group revealed reduced reactivity between immunohistochemical antibody and B cell Lymphoma 2 in comparison to the control. The administration of BFPD revealed relatively normal reactivity comparable to the control. Stereologically, HgCl2 administration also revealed a remarkable decrease in the estimated global volume of the kidney in comparison to the control while BFPD and silymarin treatment groups revealed a significant increase in global volume in comparison to the HgCl2 treated group. Antioxidant GPx gene expression of the kidney revealed the suppression of the GPx gene in the HgCl2 treated group when compared to the control. BFPD and silymarin attenuated GPx gene activity when compared to the HgCl2-treated group indicating protection against HgCl2-induced toxicity. ConclusionHence, BFPD afforded protection to the kidney against mercury-induced toxicity. The ability of BFPD to mitigate HgCl2-triggered kidney alterations could be attributed to the antioxidant property of its flavonoid content. Therefore, BFPD may be a potential candidate for treating and managing kidney-induced mercury intoxication.