期刊
INFLAMMATION RESEARCH
卷 69, 期 2, 页码 233-244出版社
SPRINGER BASEL AG
DOI: 10.1007/s00011-019-01311-2
关键词
Anti-inflammation; HO-1; MAPKs; Nf-kappa b; Rodgersia podophylla
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education [NRF-2016R1D1A3B03931713, NRF-2018R1A6A1A03024862] Funding Source: Medline
Objective Recently, Rodgersia podophylla has been reported to exhibit anti-inflammatory activity. However, little is known about the potential mechanisms about its anti-inflammatory activity. We elucidated the anti-inflammatory mechanisms of leaves extracts from Rodgersia podophylla (RP-L) in RAW264.7 cells. Materials and methods LPS-induced NO was measured by Griess and mRNA of pro-inflammatory mediators was analyzed by RT-PCR. Cell viability was measured using MTT assay. The protein level was analyzed by Western blot. Results RP-L significantly inhibited the production of the pro-inflammatory mediators such as NO, iNOS, IL-1 beta and IL-6 in LPS-stimulated RAW264.7 cells. RP-L increased HO-1 expression in RAW264.7 cells, and the inhibition of HO-1 by ZnPP reduced the inhibitory effect of RP-L against LPS-induced NO production in RAW264.7 cells. Inhibition of p38, ROS and GSK3 beta attenuated RP-L-mediated HO-1 expression. Inhibition of ROS inhibited p38 phosphorylation and GSK3 beta expression induced by RP-L. In addition, inhibition of GSK3 beta blocked RP-L-mediated p38 phosphorylation. RP-L induced nuclear accumulation of Nrf2, and inhibition of p38, ROS and GSK3 beta abolished RP-L-mediated nuclear accumulation of Nrf2. Furthermore, RP-L blocked LPS-induced degradation of I kappa B-alpha and nuclear accumulation of p65. RP-L also attenuated LPS-induced phosphorylation of ERK1/2 and p38. In GC/MS analysis of RP-L, pyrogallol was detected as bioactive compound for anti-inflammatory activity of RP-L. Pyrogallol was observed to activate HO-1 expression through ROS/GSK3 beta/p38/Nrf2/HO-1 signaling. Conclusions Our results suggest that RP-L exerts potential anti-inflammatory activity by activating ROS/GSK3 beta/p38/Nrf2/HO-1 signaling and inhibiting NF-kappa B and MAPK signaling in RAW264.7 cells. These findings suggest that RP-L may have great potential for the development of anti-inflammatory drug.
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