Kinsenoside, a high yielding constituent from Anoectochilus formosanus, inhibits carbon tetrachloride induced Kupffer cells mediated liver damage.

AIM: In the present study, we have evaluated the hepatoprotective ability of kinsenoside, a major component of Anoectochilus formosanus, in vitro and in vivo.
MATERIALS AND METHODS: The inhibitory action of kinsenoside on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells and Kupffer cells were investigated. Mice hepatic injury was produced by CCl(4) twice a week for 3 weeks. Mice in the three CCl(4) group were treated daily with water and kinsenoside throughout the experimental period.
RESULTS: In LPS-stimulated macrophage RAW 264.7 cells and Kupffer cells, kinsenoside inhibited nitric oxide (NO) production and also blocked LPS-induced inducible NO synthase expression. Furthermore, kinsenoside inhibited the NF-κB activation induced by LPS, and this is associated with the abrogation of IκBα degradation, with subsequent decreases in nuclear p65 and p50 protein levels. Moreover, the phosphorylations of p38, ERK and JNK in LPS-stimulated RAW 264.7 cells were suppressed by kinsenoside. In the in vivo study, kinsenoside significantly protected the liver from injury, by reducing the activities of plasma aminotransferase, and by improving the histological architecture of the liver. kinsenoside inhibited Kupffer cell activation by reducing the CD 14 mRNA and protein expressions.
CONCLUSION: These results indicate that kinsenoside alleviates CCl(4)-induced liver injury, and this protection is probably due to the suppression of Kupffer cell activation.