PubMed · 2017 · 17 citations · 16 references
Life SciencesImmunologyPharmacologyImmunopharmacologyInflammationInnate ImmunityAnti-inflammatory PharmacologyCytokine BiologyInflammatory Cell ResponsesInflammatory ProcessesInflammatory SignalingAnti-inflammatory ActivityAnti-inflammatory MechanismsAnti-inflammatory ResponseNf-κb SignalingNitric OxideNuclear Factor Kappa B InhibitionNuclear Factor Kappa B ModulationProstaglandin Production
), interleukin (IL)-6, and IL-1β in LPS-stimulated RAW 264.7 cells. Consistent with these observations, TTH treatment decreased the protein expression levels of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). The molecular mechanism of its anti-inflammatory activity was found to be associated with inhibition of nuclear factor-kappa B (NF-κB) phosphorylation and nuclear translocation of NF-κB 65. Furthermore, TTH markedly suppressed the LPS-induced phosphorylation of mitogen-activated protein kinases (MAPKs). Taken together, these data indicate that TTH exerts an anti-inflammatory activity by inhibiting the NF-κB and MAPK signaling pathways in LPS-stimulated RAW 264.7 cells.
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