Biologically Synthesized Gold Nanoparticles Mitigate Aluminum Chloride-Induced Nephrotoxicity via Downregulation of iNOX, LCN2 and IL-1β Genes.

Humans are constantly exposed to aluminum (Al), an environmental toxicant, and its accumulation in the glomerular could lead to acute kidney disease. Biologically synthesized gold nanoparticles (AuNPs) have been employed in the management of kidney disorders. This study assessed the modulatory effect of AuNPs mediated by Hibiscus sabdariffa (HS) on aluminum chloride (AlCl)-induced nephrotoxicity in rats. Experimental rats were randomly distributed into six groups of seven animals each. Aluminum chloride (100 mg/kg bw) was orally given to the rats for 42 days to induce nephrotoxicity. Treatment with silymarin and HS-AuNPs lasted for 14 days. Serum kidney function, tissue arginase level and oxidative stress biomarkers, as well as tissue gene expression of inducible nitric oxide synthase (iNOS), lipocalin 2 (LCN2) and interleukin-1 beta (IL-1β) were evaluated. Exposure of AlCl to the rats produced a marked (p < 0.05) increase in the levels of serum urea and creatinine in comparison with the control. Similarly, tissue arginase and malondialdehyde (MDA) levels were also increased while a reduction in the activity of superoxide dismutase (SOD) and the levels of reduced glutathione (GSH) and nitric oxide (NO) were noted in the AlCl-induced rats. Aluminum chloride also upregulated the mRNA expression of iNOS, LCN2 and IL-1β in the rats. These biochemical alterations were, however, attenuated by the administration of HS-AuNPs but the 5 mg/kg HS-AuNPs exhibited better anti-nephrotoxic activity than the 10 mg/kg dose, and could, thus serve as a potential dose for managing renal diseases.