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BackgroundLiver diseases are major global health problems. Ginseng extract has antioxidant, immune-modulatory and anti-inflammatory activities. This study investigated the effect of ginseng extract on carbon tetrachloride (CCl4)-induced liver fibrosis in rats.MethodsMale Wistar rats were divided into four groups: control group, ginseng group, CCl4 group and CCl4 + ginseng group. Liver injury was induced by the intraperitoneal (I.P) injection of 3 ml/kg CCl4 (30% in olive oil) weekly for 8 weeks. The control group was I.P injected with olive oil. The expression of genes encoding transforming growth factor beta (TGF-β), type I TGF-β receptor (TβR-1), type II TGF-β receptor (TβR-II), mothers against decapentaplegic homolog 2 (Smad2), Smad3, Smad4, matrix metalloproteinase 2 (MMP2), MMP9, tissue inhibitor matrix metalloproteinase-1 (TIMP-1), Collagen 1a2 (Col1a2), Collagen 3a1 (Col3a1), interleukin-8 (IL-8) and interleukin -10 (IL-10) were measured by real-time PCR.ResultsTreatment with ginseng extract decreased hepatic fat deposition and lowered hepatic reticular fiber accumulation compared with the CCl4 group. The CCl4 group showed a significant increase in hepatotoxicity biomarkers and up-regulation of the expression of genes encoding TGF-β, TβR-I, TβR-II, MMP2, MMP9, Smad-2,-3, -4, and IL-8 compared with the control group. However, CCl4 administration resulted in the significant down-regulation of IL-10 mRNA expression compared with the control group. Interestingly, ginseng extract supplementation completely reversed the biochemical markers of hepatotoxicity and the gene expression alterations induced by CCl4.Conclusion ginseng extract had an anti‐fibrosis effect via the regulation of the TGF‐β1/Smad signaling pathway in the CCl4‐induced liver fibrosis model. The major target was the inhibition of the expression of TGF‐β1, Smad2, and Smad3.

Silver nanoparticles (AgNPs) have attracted the most interest in terms of their potential biomedical and industrial applications. However, these nanoparticles have shown their toxic behavior toward environment, living tissues, and organisms. Selenium (Se), an essential trace element, is necessary for various metabolic processes, including protection against oxidative stress and immune function. The present study was undertaken to evaluate the effect of Se against AgNP-induced hepatic oxidative stress. AgNPs were synthesized and then prepared nanoparticles were characterized using various analytical techniques such as UV-visible spectroscopy, X-ray diffraction, and transmission electron microscopy. Rats were administered AgNPs intraperitoneally (5 mg/kg/day) and Se (0.2 mg/kg) was given by gavage. AgNP administration induced hepatic damage as indicated by the serum marker enzymes with reduction in levels of glutathione, and decrease in activities of SOD, CAT, and GSH-peroxidase ( P <0.05). Decrease in levels of total antioxidant capacity (TAC) and increase in level of C-reactive protein (CRP) was also observed in AgNP-treated group compared to control group. However, Se markedly attenuated AgNP-induced biochemical alterations, levels of TAC, CRP, and serum transaminases (AST, ALT) ( P <0.05). Taken together, these findings suggest that administration of AgNPs produces hepatotoxicity in rats, whereas Se supplementation attenuates these effects.

Zinc oxide nanoparticles (ZnONPs) are widely used in food packaging and may enter the body directly if exposed. Hereby, in this study, the oral administration was selected as the route of exposure for rats to nanoparticles and the effect of hesperidin (HSP, 100 mg/kg bwt) was evaluated on ZnONP (600 mg/kg bwt)-induced neurotoxicity in rats. ZnONPs were characterized using transmission electron microscopy. Neurotoxicity was observed as seen by elevation in serum inflammatory markers including tumor necrosis factor alpha (TNF-α), interleukin 1 (IL-1β), interleukin-6 (IL-6), C-reactive protein (CRP), and activities of catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH) content in rat brains. Pretreatment of rats with HSP in ZnONP-treated group elevated activities of antioxidant enzymes. HSP also caused decrease in TNF-α, IL-1β, IL-6, and CRP levels which was higher in the ZnONP-treated group. The results suggest that HSP augments antioxidant defense with anti-inflammatory response against ZnONP-induced neurotoxicity. The increased antioxidant enzymes enhance the antioxidant potential to reduce oxidative stress.