Over-inhibition of NADPH oxidase reduce the wound healing in liver of finfish.

Wound healing is a complex process involving soluble mediators, blood cells, extracellular matrix, and parenchymal cells in a response that occurs after surgical procedure or traumatic injury. The present study aims to investigate the ROS producing from the injury that involved in the wound healing using the ZFL (zebrafish liver cell) and tilapia partial hepatectomy model. In the ZFL, we observed that while over-inhibition of NADPH activity leading to reduce the wound healing moreover, experiment of the oxidative stress by the extracellular hydrogen peroxide exactly presented to increase the PCNA, BrdU and Ki-67 histopathological repair response of tilapia liver follow partial hepatectomy. We conclude that over inhibition of the NADPH oxidase by DPI may reduce the cell even the tissue in the progress of healing after the injury.

Studies of macrophage cellular response to the extracellular hydrogen peroxide by tilapia model.

Reactive oxygen species (ROS) may act as signaling molecules in the physiology responses and the present study aims to investigate the effect of extracellular hydrogen peroxide on macrophages cellular response. The results obtained in the present study showed that the extracellular hydrogen peroxide affectively alter the membrane potential of the cell membrane and ion exchange channels in the cell membrane through intracellular NAD turnover that may lead to an intracellular calcium ion concentration alteration and subsequently induce the downstream signal activation.