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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 HyeCha, Hee-JaeChoi, Eun OkLeem, Sun-HeeKim, Gi-YoungMoon, Sung-KwonChang, Young-ChaeYun, Seok-JoongHwang, Hye JinKim, Byung WooKim, Wun-JaeChoi, 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.
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Moon, Sung Kwon
생명공학대학 (식품영양)
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