Seon-Heui Chaa,b,c, Yongha Hwanga,b, Kil-Nam Kimd, Hee-Sook Juna,b,c,*
aCollege of Pharmacy, Gachon University, Incheon 21936, Republic of Korea
bLee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 21936, Republic of Korea
cGachon Medical and Convergence Institute, Gachon Gil Medical Center, Incheon 21565, Republic of Korea
dChuncheon Center, Korea Basic Science Institute (KBSI), Chuncheon 24341, Republic of Kore
*Corresponding author.
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-1β (IL-1β) and tumor necrosis factor-α (TNF- α), were also increased. Additionally, the mRNA expression of p65 nuclear factor-kB and I-kB-α 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.
Keywords : Zebrafish diabetic model, Free fatty acid, Infiammation, Palmitate, Fish immunology