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Orostachys japonicus  is traditionally used as an inflammatory agent. In this report, we investigated the effects of  O. japonicus  extract on the expression of genes encoding pathogen-recognition receptors (TLR2, TLR4, NOD1, and NOD2) and proinflammatory factors (iNOS, COX-2, and cytokines) in LPS-stimulated PMA-differentiated THP-1 cells and the NF- κ B and MAPK pathways.  O. japonicus  induced toxicity at high concentrations but had no effect at concentrations lower than 25  μ g/mL.  O. japonicus  inhibited LPS-induced TLR4 and NOD2 mRNA levels, suppressed LPS-induced iNOS and COX-2 transcription and translocation, and downregulated LPS-induced proinflammatory cytokine (IL-1 β , IL-6, IL-8, and TNF- α ) mRNA levels. In addition,  O. japonicus  inhibited LPS-induced NF- κ B activation and I κ B α  degradation and suppressed LPS-induced JNK, p38 MAPK, and ERK phosphorylation. Overall, our results demonstrate that the anti-inflammatory effects of  O. japonicus  are mediated by suppression of NF- κ B and MAPK signaling, resulting in reduced TLR4, NOD2, iNOS, and COX-2 expression and inhibition of inflammatory cytokine expression.

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<i>Orostachys japonicus</i>Inhibits Expression of the TLR4, NOD2, iNOS, and COX-2 Genes in LPS-Stimulated Human PMA-Differentiated THP-1 Cells by Inhibiting NF-<i>κ</i>B and MAPK Activation

Orostachys japonicusInhibits Expression of the TLR4, NOD2, iNOS, and COX-2 Genes in LPS-Stimulated Human PMA-Differentiated THP-1 Cells by Inhibiting NF-κB and MAPK Activation