Anti-inflammatory activity of the extracts from Rodgersia podophylla leaves through activation of Nrf2/HO-1 pathway, and inhibition of NF-κB and MAPKs pathway in mouse macrophage cells

被引：28

作者：

Kim, Ha Na ^{[1
]}

Kim, Jeong Dong ^{[1
]}

Park, Su Bin ^{[1
]}

Son, Ho-Jun ^{[2
]}

Park, Gwang Hun ^{[2
]}

Eo, Hyun Ji ^{[2
]}

Kim, Hyun-Seok ^{[3
]}

Jeong, Jin Boo ^{[1
,4
]}

机构：

[1] Andong Natl Univ, Dept Med Plant Resources, Andong 36729, South Korea

[2] Natl Inst Forest Sci, Forest Med Resources Res Ctr, Yongju 36040, South Korea

[3] Kyonggi Univ, Dept Food Sci & Biotechnol, Suwon 16227, South Korea

[4] Andong Natl Univ, Agr Sci & Technol Res Inst, Andong 36729, South Korea

来源：

INFLAMMATION RESEARCH | 2020年 / 69卷 / 02期

基金：

新加坡国家研究基金会;

关键词：

Anti-inflammation; HO-1; MAPKs; Nf-kappa b; Rodgersia podophylla; HEME OXYGENASE-1 EXPRESSION; AERIAL PARTS; FLAVONOL GLYCOSIDES; SIGNALING PATHWAYS; OXIDATIVE STRESS; GENE-EXPRESSION; PROTEIN-KINASE; LIPOPOLYSACCHARIDE; INFLAMMATION; INDUCTION;

D O I：

10.1007/s00011-019-01311-2

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

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.

引用

页码：233 / 244

页数：12

共 38 条

[1]

Selenium inhibits Staphylococcus aureus-induced inflammation by suppressing the activation of the NF-κKB and MAPK signalling pathways in RAW264.7 macrophages [J].