International Journal of Molecular Medicine · 2016 · 23 citations · 28 references
Life SciencesBiochemistryPharmacologyBiochemical PharmacologyImmunopharmacologyInflammationAnti-inflammatory PharmacologyBioactive Food ComponentsCytokine BiologyInflammatory Cell ResponsesInflammatory SignalingMast Cell ActivationAnti-inflammatory ActivityAnti-inflammatory MechanismsExtracellular Signal-regulated Kinase PathwayExtracellular Signal-regulated Kinase SignalingInflammatory Cytokine ProductionMitogen-activated Protein Kinase CascadesMitogen-activated Protein Kinase PathwaysPro-inflammatory Cytokine Expression
Salidroside [2-(4-hydroxyphenyl)ethyl β-D-gluco-pyranoside (SAS)] has been identified as the most potent ingredient of the plant Rhodiola rosea L. Previous studies have demonstrated that it possesses a number of pharmacological properties, including anti-aging, anti-fatigue, antioxidant, anticancer and anti-inflammatory properties. In this study, to ascertain the molecular mechanisms responsible for the anti-inflammatory activity of SAS, we used phorbol-12-myristate-13-acetate (PMA) plus A23187 to induce inflammation in human mast cell line-1 (HMC-1). The HMC-1 cells were treated with SAS prior to being stimulated with PMA plus A23187. Pro-inflammatory cytokine production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). Western blot analysis was used to examine the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB). SAS inhibited the mRNA expression and production of interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF). In cells stimulated with PMA plus A23187, SAS suppressed the phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and c-jun N-terminal kinase 1/2 (JNK1/2), but not that of p38 MAPK. SAS suppressed the expression of NF-κB in the nucleus. On the whole, our results suggest that SAS exerts an anti-inflammatory effect by inhibiting the production of pro-inflammatory cytokines through the blocking of the NF-κB and MAPK signaling pathways.
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Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis
Zhengui Xia, Martin Dickens, Joël Raingeaud et al. · Science · 1995 · 5.3K citations
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Medicine, Immunology, Pathology +17