PUBLICATION
The roles of NF-κB and ROS in regulation of pro-inflammatory mediators of inflammation induction in LPS-stimulated zebrafish embryos
- Authors
- Ko, E.Y., Cho, S.H., Kwon, S.H., Eom, C.Y., Jeong, M.S., Lee, W., Kim, S.Y., Heo, S.J., Ahn, G., Lee, K.P., Jeon, Y.J., Kim, K.N.
- ID
- ZDB-PUB-170727-8
- Date
- 2017
- Source
- Fish & shellfish immunology 68: 525-529 (Journal)
- Registered Authors
- Jeon, You-Jin
- Keywords
- Inflammation, NF-κB, Pro-inflammatory mediator, ROS, Zebrafish embryos
- MeSH Terms
-
- Zebrafish*
- Fish Proteins/metabolism*
- Fish Diseases/immunology*
- Thiocarbamates/metabolism
- NF-kappa B/metabolism*
- PubMed
- 28743626 Full text @ Fish Shellfish Immunol.
Abstract
In this study, the roles of reactive oxygen species (ROS) and NF-κB on inflammation induction in lipopolysaccharide (LPS)-stimulated zebrafish embryos were evaluated using N-acetyl-l-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), specific inhibitors of ROS and NF-κB, respectively. LPS-stimulated zebrafish embryos showed increasing production of NO and ROS and expression of iNOS and COX-2 protein, compared to a control group without LPS. However, NAC significantly inhibited production of NO and ROS and markedly suppressed expression of iNOS and COX-2 protein in LPS-stimulated zebrafish embryos. The mRNA expressions of NF-κB such as p65NF-κB and IκB-A were significantly increased after LPS stimulation, whereas PDTC attenuated mRNA expression of NF-κB. IκB was suppressed by PDTC, but not significantly. PDTC also inhibited production of NO and reduced expression of iNOS and COX-2 protein in LPS-stimulated zebrafish embryos. Taken together, these results indicated that LPS increases pro-inflammatory mediators in zebrafish embryos through ROS and NF-κB regulation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping