Anticancer Activity of Taxillus yadoriki Parasitic to Neolitsea sericea against Non-Small Cell Lung Carcinoma

Anticancer Activity of Taxillus yadoriki Parasitic to Neolitsea sericea against Non-Small Cell Lung Carcinoma

In this study, we elucidated the anti-inflammatory mechanisms of leaves extracts from Rodgersia podophylla (RPL) in RAW264.7 cells. RP-L significantly inhibited the production of the proinflammatory mediators such as NO, iNOS, IL-<TEX>$1{\beta}$</TEX> and IL-6 in LPS-stimulated RAW264.7 cells. RPL increased HO-1 expression in RAW264.7 cells, and the inhibition of HO-1 by ZnPP reduced the inhibitory effect of RPL against LPS-induced NO production in RAW264.7 cells. Inhibition of p38, ROS and <TEX>$GSK3{\beta}$</TEX> attenuated RPL-mediated HO-1 expression. Inhibition of ROS inhibited p38 phosphorylation and <TEX>$GSK3{\beta}$</TEX> expression induced by RPL. In addition, inhibition of <TEX>$GSK3{\beta}$</TEX> blocked RPL-mediated p38 phosphorylation. RPL induced nuclear accumulation of Nrf2, and Inhibition of p38, ROS and <TEX>$GSK3{\beta}$</TEX> abolished RPL-mediated nuclear accumulation of Nrf2. Furthermore, RPL blocked LPS-induced degradation of <TEX>$I{\kappa}B-{\alpha}$</TEX> and nuclear accumulation of p65. RP-L also attenuated LPS-induced phosphorylation of ERK1/2 and p38. Our results suggest that RPL exerts potential antiinflammatory activity by activating ROS/<TEX>$GSK3{\beta}$</TEX>/p38/Nrf2/HO-1 signaling and inhibiting NF-<TEX>${\kappa}B$</TEX> and MAPK signaling in RAW264.7 cells. These findings suggest that RPL may have great potential for the development of anti-inflammatory drug.