Schisandrin A suppresses lipopolysaccharide-induced inflammation and oxidative stress in RAW 264.7 macrophages by suppressing the NF-B, MAPKs and PI3K/Akt pathways and activating Nrf2/HO-1 signalingopen access
- Authors
- Kwon, Da Hye; Cha, Hee-Jae; Choi, Eun Ok; Leem, Sun-Hee; Kim, Gi-Young; Moon, Sung-Kwon; Chang, Young-Chae; Yun, Seok-Joong; Hwang, Hye Jin; Kim, Byung Woo; Kim, Wun-Jae; Choi, Yung Hyun
- Issue Date
- Jan-2018
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- schisandrin A; macrophages; inflammation; oxidative stress
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.41, no.1, pp 264 - 274
- Pages
- 11
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
- Volume
- 41
- Number
- 1
- Start Page
- 264
- End Page
- 274
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1392
- DOI
- 10.3892/ijmm.2017.3209
- ISSN
- 1107-3756
1791-244X
- Abstract
- Schisandrin A is a bioactive lignan occurring in the fruits of plants of the Schisandra genus that have traditionally been used in Korea for treating various inflammatory diseases. Although the anti-inflammatory and antioxidant effects of lignan analogues similar to schisandrin A have been reported, the underlying molecular mechanisms have remained elusive. In the present study, schisandrin A significantly suppressed the lipopolysaccharide (LPS)-induced production of the key pro-inflammatory mediators nitric oxide (NO) and prostaglandin E-2 by suppressing the expression of inducible NO synthase and cyclooxygenase-2 at the mRNA and protein levels in RAW 264.7 macrophages. Furthermore, schisandrin A was demonstrated to reduce the LPS-induced secretion of pro-inflammatory cytokines, including tumor necrosis factor- and interleukin-1; this was accompanied by a simultaneous decrease in the respective mRNA and protein levels in the macrophages. In addition, the LPS- induced translocation of nuclear factor-B (NF-B), as well as activation of mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3 kinase (PI3K)/Akt pathways were inhibited by schisandrin A. Furthermore, schisandrin A significantly diminished the LPS-stimulated accumulation of intracellular reactive oxygen species, and effectively enhanced the expression of NF erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). These results suggested that schisandrin A has a protective effect against LPS-induced inflammatory and oxidative responses in RAW 264.7 cells by inhibiting the NF-B, MAPK and PI3K/Akt pathways; these effects are mediated, at least in part, by the activation of the Nrf2/HO-1 pathway. Based on these results, it is concluded that schisandrin A may have therapeutic potential for treating inflammatory and oxidative disorders caused by over-activation of macrophages.
- Files in This Item
-
- Appears in
Collections - ETC > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1392)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.