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<p>Cadmium (Cd) is a widespread environmental pollutant that accumulates primarily in the kidneys and induces nephrotoxicity through oxidative stress, inflammation, and structural damage. Visnagin, has been reported to exhibit antioxidant and anti-inflammatory properties. This study aimed to investigate the protective effects of visnagin against cadmium-induced renal toxicity in rats.&#xa0;Twenty-eight adult Wistar albino rats were randomly assigned into four groups (<i>n</i> = 7): Control, Cadmium (Cd; 3&#xa0;mg/kg CdCl₂, i.p.), Visnagin + Cadmium (Vis + Cd; 60&#xa0;mg/kg visnagin orally + CdCl₂), and Visnagin (Vis;60&#xa0;mg/kg visnagin orally). Treatments were administered daily for 15&#xa0;days. Renal tissues were collected for histopathological examination using H&amp;E and PAS staining. To determine anti-Bax and anti-Bcl-2 immunreactivity were applied immunohistochemistry. Oxidative stress parameters (MDA, SOD, GPX1) and inflammatory cytokines (IL-1β, IL-6) were analyzed in kidney tissue by ELISA. Serum BUN and creatinine levels were measured to evaluate renal function. Data were statistically analyzed using appropriate parametric and nonparametric tests.&#xa0;Cadmium exposure caused significant renal damage, characterized by tubular dilation, glomerular atrophy, basement membrane thickening, increased inflammatory infiltration, elevated MDA, IL-1β, and IL-6 levels, reduced SOD and GPX1 activities, and increased serum BUN and creatinine levels (<i>p</i> &lt; 0.05). Visnagin treatment significantly attenuated Cd-induced histopathological alterations, suppressed oxidative stress and inflammatory responses, and improved renal function parameters. Visnagin reduced apoptotic damage by reversing CD-induced Bax increase and Bcl-2 loss.&#xa0;In conclusion, visnagin exerts a significant nephroprotective effect against cadmium-induced kidney injury through antioxidant, anti-inflammatory, and functional preservation mechanisms.</p> Graphical Abstract <p></p>

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Investigation of the protective effect of visnagin against cadmium toxicity in rat nephropathy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月14日

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  • Selim Demirtas,
  • Gul Sahika Gokdemir,
  • Ugur Seker

摘要

Cadmium (Cd) is a widespread environmental pollutant that accumulates primarily in the kidneys and induces nephrotoxicity through oxidative stress, inflammation, and structural damage. Visnagin, has been reported to exhibit antioxidant and anti-inflammatory properties. This study aimed to investigate the protective effects of visnagin against cadmium-induced renal toxicity in rats. Twenty-eight adult Wistar albino rats were randomly assigned into four groups (n = 7): Control, Cadmium (Cd; 3 mg/kg CdCl₂, i.p.), Visnagin + Cadmium (Vis + Cd; 60 mg/kg visnagin orally + CdCl₂), and Visnagin (Vis;60 mg/kg visnagin orally). Treatments were administered daily for 15 days. Renal tissues were collected for histopathological examination using H&E and PAS staining. To determine anti-Bax and anti-Bcl-2 immunreactivity were applied immunohistochemistry. Oxidative stress parameters (MDA, SOD, GPX1) and inflammatory cytokines (IL-1β, IL-6) were analyzed in kidney tissue by ELISA. Serum BUN and creatinine levels were measured to evaluate renal function. Data were statistically analyzed using appropriate parametric and nonparametric tests. Cadmium exposure caused significant renal damage, characterized by tubular dilation, glomerular atrophy, basement membrane thickening, increased inflammatory infiltration, elevated MDA, IL-1β, and IL-6 levels, reduced SOD and GPX1 activities, and increased serum BUN and creatinine levels (p < 0.05). Visnagin treatment significantly attenuated Cd-induced histopathological alterations, suppressed oxidative stress and inflammatory responses, and improved renal function parameters. Visnagin reduced apoptotic damage by reversing CD-induced Bax increase and Bcl-2 loss. In conclusion, visnagin exerts a significant nephroprotective effect against cadmium-induced kidney injury through antioxidant, anti-inflammatory, and functional preservation mechanisms.

Graphical Abstract