AI Article Synopsis
- The study investigated how reactive oxygen species (ROS) and the protein NF-κB contribute to inflammation in zebrafish embryos stimulated with lipopolysaccharide (LPS).
- LPS exposure led to higher levels of nitric oxide (NO) and ROS, as well as increased expression of inflammatory proteins iNOS and COX-2 in the embryos compared to a control group.
- The inhibitors N-acetyl-l-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) effectively reduced NO and ROS production and the inflammatory markers, showing that both ROS and NF-κB play key roles in the inflammation process induced by LPS.
Article 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. 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.
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| http://dx.doi.org/10.1016/j.fsi.2017.07.041 | DOI Listing |
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