Palmitate induces nitric oxide production and inflammatory cytokine expression in zebrafish
- Authors
- Cha, Seon-Heui; Hwang, Yongha; Kim, Kil-Nam; Jun, Hee-Sook
- Issue Date
- Aug-2018
- Publisher
- ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
- Keywords
- Zebrafish diabetic model; Free fatty acid; Inflammation; Palmitate; Fish immunology
- Citation
- FISH & SHELLFISH IMMUNOLOGY, v.79, pp.163 - 167
- Journal Title
- FISH & SHELLFISH IMMUNOLOGY
- Volume
- 79
- Start Page
- 163
- End Page
- 167
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3539
- DOI
- 10.1016/j.fsi.2018.05.025
- ISSN
- 1050-4648
- Abstract
- Inflammation markers in zebrafish embryos reflect a toxic response that is common to other animal models and humans. Free fatty acids (FFAs) are known to cause damage in various tissues by inducing inflammation. In this study, we investigated whether a FFA (palmitate) induces inflammation in zebrafish embryos. Nitrous oxide (NO) production and cyclooxygenase-2 (COX-2) mRNA expression were increased in palmitate-treated zebrafish embryos in a dose-dependent manner. mRNA expression of pro-inflammatory cytokines, interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), were also increased. Additionally, the mRNA expression of p65 nuclear factor-kB and I-kB-alpha were significantly increased after palmitate-treatment. Increased reactive oxygen species (ROS) expression was observed in palmitate-treated zebrafish embryos as well as pericardial edema. Additionally, mRNA expression of pro-inflammatory cytokines were increased in zebrafish liver and pancreas fed with palmitate-contained diet. Taken together, these results indicated that palmitate increases pro-inflammatory mediators in zebrafish embryos, suggesting that zebrafish could be an alternative animal model for inflammatory disease including diabetes.
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