Research in Pharmaceutical Sciences (Jan 2020)

Harmine protects mercuric chloride kidney-induced injury by antioxidant activity in male mice: a biochemical and histological study

  • Cyrus Jalili,
  • Nasim Akhshi,
  • Iraj Rashidi,
  • Ali Ghanbari

DOI
https://doi.org/10.4103/1735-5362.301339
Journal volume & issue
Vol. 15, no. 6
pp. 541 – 550

Abstract

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Background and purpose: Mercuric chloride (Merc) can cause kidney toxicity. Harmine (Harm), an herbal alkaloid has various pharmacological and medicinal effects mainly because of its antioxidant activity. In this study, therefore, Harm's protective mechanisms on Merc-induced nephrotoxicity in BALB/c male mice were investigated. Experimental approach: Forty-eight male mice were randomly divided into six groups (n = 8). Groups were received saline, Merc (0.5 mL/day of 0.5 ppm aqueous), Harm (5, 10, 15 mg/kg/day), Merc + Harm (5, 10, 15 mg/kg/day) for 14 consecutive days. Saline and Harm were administrated intraperitoneally and Merc dissolved in drinking water. Urea and creatinine serum levels, body weight, kidney weight, quantitative and qualitative histological alterations, apoptosis rate, total antioxidant capacity (TAC), superoxide dismutase (SOD), and nitric oxide (NO) levels were evaluated. Findings/Results: There was a significant reduction in total body and kidney weights, renal histological criteria, TAC, SOD levels in the Merc group compared to the control group (P < 0.05), whereas these parameters in the Merc + Harm groups, were significantly increased compared to the Merc group (P < 0.05). Urea and creatinine serum levels, levels of NO, and apoptosis were significantly higher in the Merc group than the control, while these parameters were decreased in the Merc + Harms groups in comparison with the Merc group (P < 0.05). Conclusion and implications: Harm protected Merc-induced renal damage in mice. This protection was observed in both histological and biochemical respects. The beneficial effect of Harm was related to its antioxidant properties that diminish NO production and apoptosis induction in the kidney.

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