Abstract
The aim of the present study is to illustrate the effects of swertiamarin (STM), a natural iridoid from herbal medicines, on hepatic inflammation induced by carbon tetrachloride (CCl4) in rats. Male Sprague Dawley rats were exposed to CCl4 with or without STM co-administration for 8 weeks. Our results revealed that STM administration (100 and 200 mg/kg b.w.) significantly attenuated inflammation in livers of CCl4-treated rats. STM remarkably reduced the production of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), macrophage inflammatory protein-1a (MIP-1α), and monocyte chemotactic protein-1 (MCP-1) in liver tissue of CCl4-treated rats. In addition, STM treatment downregulated connective tissue growth factor (CTGF) and ser307pIRS-1 expression, which was induced by CCl4 exposure. In the process of exploring the anti-inflammatory mechanisms of STM action, we demonstrated that STM significantly inhibited Toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) p65 expression in the liver. In conclusion, these results suggested that the inhibition of CCl4-induced inflammation by STM was, at least in part, due to its regulation of the TLR4 /NF-κB signaling pathway.
Highlights
Swertiamarin (STM) is a bitter secoiridoid glycoside isolated from gentianaceae medicinal plants exerting notable hepatoprotective effects (Jaishree, Badami 2010; Zhang et al, 2015)
Tissue damage associated with hepatic inflammation can be mediated by the proinflammatory cytokines such as inducible nitric oxide synthase, interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α)
The nuclear factor kappa B (NF-κB) is one of the most ubiquitous transcription factors modulating the immune response to infection or stimuli (Tornatore et al, 2012)
Summary
Swertiamarin (STM) is a bitter secoiridoid glycoside isolated from gentianaceae medicinal plants exerting notable hepatoprotective effects (Jaishree, Badami 2010; Zhang et al, 2015). Tissue damage associated with hepatic inflammation can be mediated by the proinflammatory cytokines such as inducible nitric oxide synthase, interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) (Ma et al., 2014). These cytokines can stimulate the Kupffer cells to release various inflammatory mediators and free radicals (Decker 1990). In response to stimulation of external risk factors, tissues engage the innate immune response and up-regulate TLR4 expression. Various signaling molecules have been shown to regulate the TLR pathway to modulate innate immune responses (Fang et al, 2016). NF-κB and TLRs have attracted interest as targets for the treatment of inflammatory liver damage (Shin et al, 2013; Ma et al, 2015)
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