| dc.description.abstract | Objective: Drug induced hepatocyte death is a major contributor to acute liver failure. We aimed to deter-
mine whether b-sitosterol conjugated silver nanoparticles (BSAgNPs) could ameliorate carbon tetrachlo-
ride (CCl4)-induced liver injury in Swiss albino mice.
Methods: Biogenic silver nanoparticles were synthesized from b-sitosterol to produce b-sitosterol (BS)
conjugated silver nanoparticles. Serum liver function assays in mice model with CCl4-induced liver injury
revealed that alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase
(ALP), bilirubin and cholesterol levels decreased markedly after treatment with b-sitosterol and
BSAgNPs. In vivo liver enzymatic assays, including superoxide dismutase (SOD), catalase and reduced glu-
tathione (GSH) were conducted to assess the antioxidant activity of the treatments.
Results: Liver tissue from BSAgNP treated mice displayed significantly elevated SOD activity (73.57 ± 1.
48%) when compared to positive control group with silymarin treatment. Catalase activity decreased
drastically in CCl4 treated mice (47.14 ± 1.08%), but increased with the administration of BSAgNPs (72.
24 ± 2.25%). An increase in transforming growth factor b (TGF-b1) in liver tissue homogenate accompa-
nied a reduction in nuclear factor erythroid-2-related factor 2 (Nrf2) in CCl4 treated mice. b-sitosterol and
BSAgNPs mediated the reduction of TGF-b1. In the BSAgNPs treated mice, Nrf2 level was significantly ele-
vated; however, no change was detected following b-sitosterol treatment.
Conclusion: Our findings reveal that b-sitosterol conjugated silver nanoparticles (BSAgNPs) may cause
activation of the Nrf2 gene, through potential inhibition of TGF b1/Smad signaling. Antifibrotic effect
of BSAgNPs may promote the lowering of chronic inflammation, oxidative stress and collagen deposition.
Nanoparticle-mediated drug delivery of b-sitosterol may therefore have therapeutic promise against hep-
atic complications. | en_US |
