The Effect Of TXNIP In Renal Ischemia/Reperfusion In Jury Inmice

Objective:Ischemia/reperfusion(I/R)injury is a common cause of acute kidney injury,and oxidative stress plays an important role in the development of acute kidney injury.Thioredoxin interaction protein(TXNIP)can regulate intracellular oxidative stress.The aim of this study was to investigate the expression of TXNIP,the effect of TXNIP knockout on renal tissue oxidative stress,apoptosis and proliferation induced by ischemia-reperfusion,to provide an experimental theory for the pathogenesis and treatment target of perfusion injury.Methold:TXNIP knockout(TKO)mice were used to construct a mouse model of renal ischemia-reperfusion injury.Immunohistochemistry and western blot were used to detect the expression of TXNIP in renal of ischemia-reperfusion mice.The effect of TXNIP knockout on oxidative stress,apoptosis and proliferation-related markers after renal ischemia-reperfusion was detected.Result:After renal ischemia-reperfusion for 24 h,the expression of TXNIP began to increase and insistent to 14 days.After renal ischemia-reperfusion for 48 h,the level of serum creatinine and urea nitrogen was increased,renal tubular epithelial cells shed,cell-like necrosis occurred,cell debris tube type visible,apoptosis increased,proliferation decreased and oxidative damage increased in renal tissues of I/R group.Knockout of TXNIP decreased serum creatinine and urea nitrogen levels,renal tubular epithelial cell lesions and apoptosis.Bax and cleaved caspase-3 expression was decreased,Bcl-2 and Ki-67 expression was increased,8-OHdG and NOX4 expression was down-regulated in renal tissues of TKO+ I/R group.Conclusion:1.The expression of TXNIP is up-regulate in renal of I/R.2.Knockout of TXNIP significantly improve I/R-induced renal dysfunction and reduce renal disease.3.Knockout of TXNIP inhibit I/R-induced apoptosis and promote cell proliferation.4.Knockout of TXNIP significantly improved I/R-induced oxidative stress.