Abstract
The current study was designed to investigate the anti-inflammatory effect of salidroside (SDS) and the underlying mechanism by using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages in vitro and a mouse model of binge drinking-induced liver injury in vivo. SDS downregulated protein expression of toll-like receptor 4 (TLR4) and CD14. SDS inhibited LPS-triggered phosphorylation of LPS-activated kinase 1 (TAK1), p38, c-Jun terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Degradation of IκB-α and nuclear translocation of nuclear factor (NF)-κB were effectively blocked by SDS. SDS concentration-dependently suppressed LPS mediated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein levels, as well as their downstream products, NO. SDS significantly inhibited protein secretion and mRNA expression of of interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Additionally C57BL/6 mice were orally administrated SDS for continuous 5 days, followed by three gavages of ethanol every 30 min. Alcohol binge drinking caused the increasing of hepatic lipid accumulation and serum transaminases levels. SDS pretreatment significantly alleviated liver inflammatory changes and serum transaminases levels. Further investigation indicated that SDS markedly decreased protein level of IL-1β in serum. Taken together, these data implied that SDS inhibits liver inflammation both in vitro and in vivo, and may be a promising candidate for the treatment of inflammatory liver injury.
Highlights
Inflammation is an early response to tissue injury and foreign pathogens, and the normal tissue structure and function are recovered
Our results confirmed that phosphorylation of extracellular signal-regulated kinase (ERK), Jun terminal kinase (JNK), and p38 mitogen-activated protein kinases (MAPKs) were significantly increased by treatment with LPS
Binge drinking can create an inflammatory response in the liver, so we investigated the contribution contribution of SDS to alcohol-induced liver injury in vivo in a model of acute alcohol intoxication of SDS to alcohol-induced liver injury in vivo in a model of acute alcohol intoxication caused by binge caused by binge drinking
Summary
Inflammation is an early response to tissue injury and foreign pathogens, and the normal tissue structure and function are recovered. A normal inflammatory response regulates expression of pro-inflammatory and anti-inflammatory proteins. During these inflammation responses macrophages are essential cells that bridged innate and adaptive immunity. IκB the is undergoing phosphorylation binds to DNA and induces further pro-inflammatory gene expression and inflammatory response [3,4]. The mitogen-activated kinases (MAPKs) are a afamily of serine/threonine protein kinases, the inhibition ofprotein the NF-κB pathway may have beneficial effect in anti-inflammation. MAPKs signaling pathways the synthesis and release of pro-inflammatory (ERK) andofp, playing an essential role inleads in thetoregulation of cellular responses to cytokines and mediators macrophages the inflammatory response stresses by [5].activated. Several references have reported that SDS regulated cytokine through the MAPK/NF-κB pathway [18].
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