Inhibitory effects of diallyl sulfide on the activation of Kupffer cell in lipopolysaccharide/d-galactosamine-induced acute liver injury in mice

[Display omitted] •The hepatoprotective effects of diallyl sulfide and GdCl3 on acute liver injury.•Diallyl sulfide suppressed the activation of Kupffer cell in liver injury.•Diallyl sulfide inhibited the production and secretion of proinflammatory mediators.•Diallyl sulfide failed to increase the p...

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Veröffentlicht in:Journal of functional foods 2019-11, Vol.62, p.103550, Article 103550
Hauptverfasser: Li, Ming, Wang, Shuo, Li, Xianjie, Wang, Qiong, Liu, Zhidan, Yu, Ting, Kou, Ruirui, Xie, Keqin
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Sprache:eng
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Zusammenfassung:[Display omitted] •The hepatoprotective effects of diallyl sulfide and GdCl3 on acute liver injury.•Diallyl sulfide suppressed the activation of Kupffer cell in liver injury.•Diallyl sulfide inhibited the production and secretion of proinflammatory mediators.•Diallyl sulfide failed to increase the production of IL-10 in acute liver injury. Diallyl sulfide (DAS) is an effective bioactive organosulfur compound extracted from garlic. This study aimed to explore whether the protective effect of DAS on lipopolysaccharide (LPS)/d-galactosamine (d-GalN) induced acute liver injury was associated with the regulation of Kupffer cell (KC) activation. The results indicated that DAS administration protected mice from LPS/D-GalN-induced histopathological damage and serum aminotransferase elevation and also showed more pronounced beneficial effects than GdCl3 administration. The F4/80+ or CD11b+ KC immunohistochemistry results showed that DAS administration suppressed LPS/D-GalN-induced KC activation. DAS administration also suppressed LPS/D-GalN-triggered production of TNF-α, IL-1β, MCP-1 and NO in the liver or serum, which was in line with the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1 and iNOS in the liver. Taken together, these findings reveal that the protective effects of DAS on LPS/D-GalN-induced acute liver injury may be achieved by inhibiting the activation of KC, thereby suppressing the secretion of various proinflammatory mediators.
ISSN:1756-4646
2214-9414
DOI:10.1016/j.jff.2019.103550