β-Caryophyllene downregualtes inflammatory cytokine expression and alleviates systemic inflammation in mice by inhibiting the NF-κB signaling pathway
Objective To investigate the anti-inflammatory mechanism of β-caryophyllene(BCP)on lipopolysaccharide(LPS)-induced systemic inflammation in mice.Methods C57BL mice were divided into control group,LPS-treated group,dexamethasone-treated group,and BCP-treated group.Twelve hours after the establishment of the whole body inflammation model by intraperitoneal injection of LPS,the serum levels of interleukin 1β(IL-1β),tumor necrosis factor α(TNF-α),and IL-6 were measured by ELISA.The protein levels of nuclear factor κB p65(NF-κB p65),myeloid differentiation primary response 88(MyD88),and Toll-like receptor 4(TLR4)in spleen tissue were assessed by Western blot analysis.Results Compared with the control group,the serum levels of the inflammatory cytokines IL-1β,TNF-α and IL-6 in the LPS-treated group were significantly increased.In addition,the pro-tein levels of NF-κB p65,MyD88 and TLR4 were increased in spleen tissues.Compared with the LPS-treated group,the protein levels of IL-1β,TNF-α and IL-6 in the BCP-treated group were decreased significantly.Furthermore,the protein levels of NF-κB p65,MyD88 and TLR4 in spleen tissue showed a remarkable reduction.The inhibitory effect was notably better in the 3.5 μg/(L·d)BCP-treated group than in the 3 μg/(L·d)BCP-treated group.Conclusion BCP exerts anti-inflammatory effects by downregulating inflammatory cytokine expression through the inhibition of the NF-κB signaling pathway.
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