Vanillic acid, agmatine, and silver nanoparticles enhanced Nrf2 pathway and inhibited inflammatory, apoptotic, and fibrotic signaling in cadmium-induced nephrotoxicity in rats.

OBJECTIVE

The purpose of this study is to examine the renoprotective, antioxidant, and anti-inflammatory properties of silver nanoparticles (AgNPs), vanillic acid, and agmatine against cadmium chloride-induced nephrotoxicity in rats.

METHODS

Ninety-six male rats were randomly allocated into eight groups (12 rats each): a normal control group; a cadmium chloride (CdCl₂, 2 mg/kg, i.p.) group; a CdCl₂ + AgNPs group (2.5 mg/kg, orally); a CdCl₂ + vanillic acid group (200 mg/kg, orally); a CdCl₂ + agmatine group (100 mg/kg, i.p.); a CdCl₂ + AgNPs + vanillic acid group; a CdCl₂ + AgNPs + agmatine group; and a CdCl₂ + vanillic acid + agmatine group. All rats were sacrificed at 8th day of the CdCl₂ injection. Kidney function tests (creatinine and urea levels), oxidant/antioxidant parameters (malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activity), and the expression of genes (TNF-α, IL-6, BAX, Nrf2, TGF-β, and aquaporin-1 (AQP-1)) were evaluated in the kidney tissues.

RESULTS

CdCl₂ significantly elevated urea, creatinine, MDA, TNF-α, IL-6, BAX, and TGF-β levels while reducing SOD, catalase, Nrf2, and AQP-1 expression compared to the normal group. In comparison to the CdCl₂ group, vanillic acid, agmatine, and AgNPs increased the levels of SOD, GSH, catalase, Nrf2, and AQP-1 while decreasing those of urea, creatinine, MDA, TNF-α, IL-6, BAX, and TGF-β.

CONCLUSION

the effective renoprotective, antioxidant, and anti-inflammatory qualities of vanillic acid, agmatine, and AgNPs against CdCl₂-induced nephrotoxicity suggest their potential as treatment agents for kidney damage caused by cadmium chloride.