TY - JOUR
T1 - Kinsenoside isolated from anoectochilus formosanus suppresses LPS-stimulated inflammatory reactions in macrophages and endotoxin shock in mice
AU - Hsiao, Hung Bo
AU - Wu, Jin Bin
AU - Lin, Ho
AU - Lin, Wen Chuan
PY - 2011/2
Y1 - 2011/2
N2 - 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-α, IL-1β, monocyte chemoattractant protein 1, and macrophage migration inhibitory factor production. Furthermore, kinsenoside decreased the formation of a nuclear factor κB-DNA complex and nuclear p65 and p50 protein levels. Kinsenoside inhibited nuclear factor κB translocation through both IκBα-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-α, IL-1β, 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.
AB - 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-α, IL-1β, monocyte chemoattractant protein 1, and macrophage migration inhibitory factor production. Furthermore, kinsenoside decreased the formation of a nuclear factor κB-DNA complex and nuclear p65 and p50 protein levels. Kinsenoside inhibited nuclear factor κB translocation through both IκBα-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-α, IL-1β, 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.
KW - Cytokine
KW - LPS
KW - inflammation
KW - kinsenoside
UR - http://www.scopus.com/inward/record.url?scp=78751632879&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78751632879&partnerID=8YFLogxK
U2 - 10.1097/SHK.0b013e3181f0e7a3
DO - 10.1097/SHK.0b013e3181f0e7a3
M3 - Article
C2 - 20661184
AN - SCOPUS:78751632879
SN - 1073-2322
VL - 35
SP - 184
EP - 190
JO - Shock
JF - Shock
IS - 2
ER -