In the present study, we reported that
kinsenoside, a major component of Anoectochilus formosanus, inhibited inflammatory reactions in mouse peritoneal lavage macrophages and protects mice from
endotoxin shock. In LPS-stimulated mouse peritoneal lavage macrophages,
kinsenoside inhibited the inflammatory mediators, such as
nitric oxide,
TNF-[alpha], IL-1[beta],
monocyte chemoattractant protein 1, and
macrophage migration inhibitory factor production. Furthermore,
kinsenoside decreased the formation of a
nuclear factor [kappa]B-
DNA complex and nuclear p65 and p50
protein levels.
Kinsenoside inhibited
nuclear factor [kappa]B translocation through both
I[kappa]B[alpha]-dependent and -independent pathway. In contrast, it stimulated anti-inflammatory
cytokine IL-10 generation and enhanced the
mRNA expression of
IL-10 and suppressor of
cytokine signaling 3 in the same cells induced by LPS. In an animal model, both pretreatment and posttreatment of
kinsenoside increased the survival rate of ICR mice challenged by LPS (80 mg/kg, i.p.). Pretreatment with
kinsenoside decreased serum levels of
TNF-[alpha], IL-1[beta],
IL-10,
monocyte chemoattractant protein 1, and migration inhibitory factor at 1 h after sublethal dose of LPS (40 mg/kg, i.p.) in mice. In contrast,
kinsenoside enhanced serum
IL-10 level at 24 h after LPS injection in mice. In conclusion,
kinsenoside inhibited the production of inflammatory mediators and enhanced anti-inflammatory
cytokine generation. Therefore,
kinsenoside can alleviate acute inflammatory hazards.