Expression Of CXCL9 And FKN During Pulmonary Ischemia Reperfusion Injury In Rats

Background:Pulmonary ischemia-reperfusion injury(PIRI). In recent years,along with surgery and lung preservation of the rapid development of medicaltechnology with thrombolysis drug development, the lung trans-plant and fibrinolytictherapy has become effective treatments for most end-stage lung diseases andpulmonary embolism, but the main means PIRI is always affect thrombolysis and theprognosis after transplantation is an important factor.objective: To investigate the expression of CXCL9 and FKN in lung ischemiareperfusion injury in rats and the effect of IMD1-53 on them.Methods: Rat lung model of ischemia reperfusion injury was established invivo.Seventh-two healthy wistar rats were randomly divided into threegroups:surgical control(group C),ischemia reperfution group(IR group), IMD1-53group(IMD group).In group C,the rats only had a thoracotomy, In IR group, onemilliliters of saline solution was administered intraperi- toneally 2 h prior tooperation.then their right lungs underwent 90 min ischemia, followed by 60 min and120 min of reperfusion.In IMD group,IMD1-53 was injected intraperitoneally2nmol/kg 2h prior to opera- tion,the following experimental protocol was the same asthat of the IR group. The unilateral pulmonary ischemia-reperfusion model wasreplicat- ed. The plasma sample and the right lung were collected at different threetime spots:45min ischemia,60 min and 120min reperfusion ( 8 rats in eachgroups).The plasma contents of CXCL9 was determined by ELISA, and theexpression of FKN in lung tissue were detected by immunohistolchemistry. The lungtissue injury was evaluated by histology.Result: 1.The plasma contents of CXCL9:The plasma contents of IR group ineach time were higher than that in group C(P<0.05),but the contents of IMD group ineach time were significantly lower than in IR group (P<0.05).2.The expression ofFKN in lung:the expression of FKN in IR group was higher than group C(P<0.05),that in IMD group was signify- cantly lower than IR group(P<0.05).3.histology change:Appear capillaryes, alveolar edema,inflammatory cells infiltration. With theextension of time,the reperfusion injury accentuate further, alveolar cavity drainage.Prepreamented by IMD 1-53, the lung tissue injury was descended.Conclusions: IMD1-53 treatment before ischemia can protect the lung tissueagainst ischemia reperfusion injury possibly by reduce CXCL9 and FKN expression.