DNA Repair Effect Of Ref-1 In Post-ischemia Reperfusion Injury Of Liver, Kidey, Small Intestine And Lung After Rat Liver Transplantation

Since the first successful liver transplantation in an adult patientwas reported, the number of liver transplantation has steadilyincreased,so that this modality has become established as a standardsurgical method for the treatment of late-stage liverdiseases.Currently, for the sake of liver transplantation is thecomplication of liver and kidney and small intestine and lung. The liver transplantation result to reperfused tissue, oxide stressis recongnized as a critical cause of injury in reperfused tissue.Accumulated data from many studies currently suggest thatintracellular as well as extracellular oxidative stress may play animportant role in inducing postischemic tissue injury. At a veryearlyphase of reperfusion, production of reactive oxygen species(ROS) associated with Rac1 has recently been reported to mediateintracellular oxidative stress. ROS generation in the postischemictissure injury. Therefore, regulating the cellular redox state bysuppressing cellular ROS in the postischemic tissue is likely to becrucial for protection against ischemia/reperfusion (I/R) inducedliver injury.Redox factor-1 (Ref-1) has been showed to function in aredox-dependent manner in the cell.the study was designed toexamine the effects of Ref-1 on liver transplantation as well asprotection against postischemic injury in a ray model of livertransplantation in rat. Redox factor-1 successfully expressed in theliver and kidney and small instine and lung. Redox factor-1 alsoreduceded post-transplantation injury and inflammatory reactions inthe grafts. The results of the present study may open a new avenue totreatment of ischemia/reperfusion in liver transplantation.