Large yellow croaker peroxiredoxin IV protect cells against oxidative damage and apoptosis.

Oxidative stress and inflammation lead to cell damage and are implicated in many disease states. High concentrations of hydrogen peroxide (H2O2) may mediate cells apoptosis by increasing intracellular reactive oxygen species (ROS) levels. In this study, we established a LYCK-PrxIV cell line (large yellow croaker head kidney cell line stably expressing peroxiredoxin IV). The level of nitric oxide (NO), superoxide anion and hydrogen peroxide (H2O2) in this LYCK-PrxIV cells were significantly lower than those in control cells of LYCK-pcDNA3.1 (LYCK cell line stably transfected by pcDNA3.1 vector). Additionally, when exposed to H2O2, cell apoptosis was significantly alleviated in LYCK-PrxIV than in control cells. Meanwhile, the ROS level and ATP content were maintained more stable in LYCK-PrxIV than in LYCK-pcDNA3.1. The over-expression of LcPrxIV in LYCK-PrxIV cells induced a declined mRNA expression of LcCXC, LcCC, LcIL-8 and LcTNF-α2, as well as an increase of LcIL-10 mRNA expression, when compared to LYCK-pcDNA3.1. On the other hand, the expression of chemokine LcCXC, LcCC and LcTNF-a2 increased in LYCK-pcDNA3.1 after H2O2 stimulation, while that of LcIL-8 and LcIL-10 decreased. The regualtion of gene expression in LYCK-PrxIV cells was almost the same as that in LYCK-pcDNA3.1, but the change fold was much more moderate. These results suggest that LcPrxIV may be an indispensable ROS scavenger protecting LYCK cells against oxidative damage as well as the subsequent apoptosis and inflammatory response, which provides a clue that LcPrxIV may be an assist in fish immune response.