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Lycopene suppresses LPS-induced NO and IL-6 production by inhibiting the activation of ERK, p38MAPK, and NF-kappa B in macrophages

Feng, Dan ; Ling, Wen-Hua and Duan, Rui-Dong LU (2010) In Inflammation Research 59(2). p.115-121
Abstract
Lycopene has antioxidant, anticancer, and anti-inflammatory effects with molecular mechanisms not fully identified. We investigated the effects of lycopene on the inflammatory responses to lipopolysaccharide (LPS) in RAW264.7 cells and the signal transduction pathways involved. Lycopene inhibited LPS-induced production of nitric oxide (NO) and interleukin-6 (IL-6) with decreased mRNAs of inducible nitric oxide synthase and IL-6 but had no effect on TNF-alpha. Further study showed that lycopene also inhibited LPS-induced I kappa B phosphorylation, I kappa B degradation, and NF-kappa B translocation. Moreover, lycopene blocked the phosphorylation of ERK1/2 and p38 MAP kinase but not c-Jun NH2-terminal kinase. To confirm the causal link... (More)
Lycopene has antioxidant, anticancer, and anti-inflammatory effects with molecular mechanisms not fully identified. We investigated the effects of lycopene on the inflammatory responses to lipopolysaccharide (LPS) in RAW264.7 cells and the signal transduction pathways involved. Lycopene inhibited LPS-induced production of nitric oxide (NO) and interleukin-6 (IL-6) with decreased mRNAs of inducible nitric oxide synthase and IL-6 but had no effect on TNF-alpha. Further study showed that lycopene also inhibited LPS-induced I kappa B phosphorylation, I kappa B degradation, and NF-kappa B translocation. Moreover, lycopene blocked the phosphorylation of ERK1/2 and p38 MAP kinase but not c-Jun NH2-terminal kinase. To confirm the causal link between MAP kinase inhibition and its anti-inflammatory effects, we treated the cells with SB 203580 and U0126. These inhibitors significantly inhibited LPS-induced NO and IL-6 formation. Lycopene inhibits the inflammatory response of RAW 264.7 cells to LPS through inhibiting ERK/p38 MAP kinase and the NF-kappa B pathway. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
ERK1/2, p38 MAP kinase, Nitric oxide, Lycopene, Interleukin-6
in
Inflammation Research
volume
59
issue
2
pages
115 - 121
publisher
Birkhäuser Verlag
external identifiers
  • wos:000273787200004
  • scopus:77949270779
  • pmid:19693648
ISSN
1420-908X
DOI
10.1007/s00011-009-0077-8
language
English
LU publication?
yes
id
14c3d0f4-cf99-48e6-946f-8df07ac9b9c2 (old id 1547296)
date added to LUP
2016-04-01 10:19:09
date last changed
2020-08-09 03:15:17
@article{14c3d0f4-cf99-48e6-946f-8df07ac9b9c2,
  abstract     = {Lycopene has antioxidant, anticancer, and anti-inflammatory effects with molecular mechanisms not fully identified. We investigated the effects of lycopene on the inflammatory responses to lipopolysaccharide (LPS) in RAW264.7 cells and the signal transduction pathways involved. Lycopene inhibited LPS-induced production of nitric oxide (NO) and interleukin-6 (IL-6) with decreased mRNAs of inducible nitric oxide synthase and IL-6 but had no effect on TNF-alpha. Further study showed that lycopene also inhibited LPS-induced I kappa B phosphorylation, I kappa B degradation, and NF-kappa B translocation. Moreover, lycopene blocked the phosphorylation of ERK1/2 and p38 MAP kinase but not c-Jun NH2-terminal kinase. To confirm the causal link between MAP kinase inhibition and its anti-inflammatory effects, we treated the cells with SB 203580 and U0126. These inhibitors significantly inhibited LPS-induced NO and IL-6 formation. Lycopene inhibits the inflammatory response of RAW 264.7 cells to LPS through inhibiting ERK/p38 MAP kinase and the NF-kappa B pathway.},
  author       = {Feng, Dan and Ling, Wen-Hua and Duan, Rui-Dong},
  issn         = {1420-908X},
  language     = {eng},
  number       = {2},
  pages        = {115--121},
  publisher    = {Birkhäuser Verlag},
  series       = {Inflammation Research},
  title        = {Lycopene suppresses LPS-induced NO and IL-6 production by inhibiting the activation of ERK, p38MAPK, and NF-kappa B in macrophages},
  url          = {http://dx.doi.org/10.1007/s00011-009-0077-8},
  doi          = {10.1007/s00011-009-0077-8},
  volume       = {59},
  year         = {2010},
}