SILDENAFIL DECREASED TNF-α AND IL-6 LEVELS IN CD‐INDUCED ACUTE TOXICITY

Objective: This study aimed to evaluate the effects of sildenafil (SIL) on inflammation and histopathological changes in cadmium (Cd)-induced toxicity in female rats. Material and Method: Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF- α) levels were measured to assess the degree of inflammation. Histopathological changes in the liver, lungs and kidneys were also assessed. Result and Discussion: SIL significantly reduced the cellular release of TNF-α and IL-6, which have been implicated in the pathogenesis of Cd-induced tissue damage. When SIL was administered alone, it showed histopathological effects similar to the control group. However, it was found that co-administration of SIL with Cd prevented portal vein dilation and central vein enlargement in the liver, prevented necrosis in kidney tissue, but did not affect the lung. Although SIL has variable protective effects on tissues, our results are in support of the idea that the use of SIL in tissue damage management can be investigated for its efficacy in modulating oxidative stress-induced proinflammatory cytokine activation in vivo and ultimately help prevent Cd-induced tissue damage. Our study has shown that SIL can reduce Cd-induced acute toxicity in rats. SIL may be use as a protective agent against toxicity of heavy metals.