The Protective Role Of Ischemic Preconditioning On Acute Kidney Injury And Renal Fibrosis In Rat

Acute kidney injury(AKI)is a clinical syndrome characterized by a sharp decrease in glomerular filtration rate(GFR)in a short time,which is caused by ischemia,sepsis and nephrotoxic drugs.In recent years,with the improvement of medical means and nursing technology,the incidence of AKI has increased year by year,and the mortality rate of patients remains high.Long-term clinical follow-up study found that AKI was an independent risk factor for chronic kidney disease(CKD)and end-stage renal disease(ESRD).AKI patients were much more likely to develop CKD after discharge than those without AKI.CKD is a chronic disease with high incidence and hidden condition,which seriously endangers human health.Its characteristic pathological changes are the formation of renal fibrosis.A large number of collagen fibers are deposited in the glomeruli and interstitium,which seriously affects the normal function of the kidney.Recently,it has progressed to ESRD.Therefore,it is an urgent problem in the field of Nephrology to explore the pathological mechanism of AKI,to find effective ways to promote the recovery of renal tissue structure and function after injury and to slow down the formation of renal fibrosis after injury.Current studies have found that ischemic preconditioning(IPC),i.e.multiple short reperfusion/ischemia treatments before ischemia,can delay and alleviate reperfusion injury,but the protective mechanism is still unclear.In addition,the role of IPC in renal fibrosis after AKI needs to be further explored.In this study,we used renal artery occlusion for 50 minutes to establish renal ischemia reperfusion(I/R)injury model in male SD rats.SD rats were randomly divided into three groups: sham group,ischemia reperfusion(I/R)group and ischemic preconditioning(IPC)group.Two days after the establishment of animal models,the concentration of creatinine and urea nitrogen in serum was detected,and the kidney tissues were observed by HE staining to identify the degree of kidney injury in each group.At the same time,immunological and molecular biological techniques were used to explore the protective effects of IPC on renal injury.In addition,the deposition of collagen fibers in kidney tissues was detected 30 days after model establishment,and the effect of IPC on renal fibrosis was observed.The results show that IPC can reduce the oxidative damage of mitochondrial DNA and proteins by inhibiting the production of ROS in mitochondria after acute renal injury,thereby reducing the apoptosis and necrosis of renal cells after injury,and protecting the morphology and function of kidney in acute renal injury induced by I/R.At the same time,IPC can also inhibit the formation of renal fibrosis after injury by regulating the expression of transforming growth factor TGF-?1.This study provides a theoretical reference for the clinical application of IPC,and provides a new research idea for the prevention and treatment of fibrosis after renal injury.