Protective Role of Silymarin and Deferoxamine Against Iron Dextran‑induced Renal Iron Deposition in Male Rats

Mehdi Nematbakhsh, Zahra Pezeshki, Behjat-Alsaadat Moayyedi, Fatemeh Eshraghi-Jazi, Ardeshir Talebi, Hamid Nasri, Shahrzad Baradaran, Marjan Gharagozloo, Tahereh Safari, Maryam Haghighi


 Background: Kidney iron deposition (KID) is caused by iron overload that is observed in kidney diseases and anemia. The protective effects of deferoxamine (DF) and silymarin (SM) were studied against iron overload‑induced KID in rat model.

Methods: Rats received iron dextran (200 mg/kg) for a period of 4 weeks every other day, but at the beginning of week 3, they also were subjected to a 2‑week (every other day) treatment with vehicle (group 2, positive control), SM (200 mg/kg; group 3), DF (50 mg/kg; group 4), SM (400 mg/kg; group 5), and combination of SM and DF (200 and 50 mg/kg, respectively; group 6). Group 1, as the negative control, received saline alone during the study. The levels of serum creatinine (Cr), blood urea nitrogen (BUN), iron, ferritin, and nitrite were determined, and the kidney was removed for histopathological investigations.

Results: Before treatment, the serum levels of iron and ferritin in all iron dextran receiver groups were significantly higher than those of the negative control group (P < 0.05). However, the serum levels of BUN, Cr, and nitrite were not different between the groups. No statistical differences were detected in kidney weight and the serum levels of BUN, Cr, iron, ferritin, and nitrite after 2 weeks of treatment with SM, DF, or combination of both. The SM and DF treatments reduced the intensity of the KID, but only in the SM (200 mg/kg) group, a significant reduction in KID was observed (P < 0.05).

Conclusion: It seems that SM is a nephroprotectant agent against KID in acute iron overload animal models.

Keywords: Deferoxamine, iron overload, kidney iron deposition, silymarin

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