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Effects Of Hyperbaric Oxygen On The Expression Of RIP-1 And RIP-3 In Renal Tissues Of Rat After Renal Transplantation Ischemia Reperfusion

Posted on:2019-08-18Degree:MasterType:Thesis
Country:ChinaCandidate:H LiFull Text:PDF
GTID:2394330566969259Subject:Surgery
Abstract/Summary:PDF Full Text Request
Objective: Using renal transplantation to establish a rat renal ischemia reperfusion injury(IRI)model.To detect the receptor-interacting protein kinase 1(RIP-1)and receptor-interacting protein kinase 3(RIP-3),a key signaling factor of necroptosis.Observed after hyperbaric oxygenation(HBO)treatment effects on the expression of RIP-1and RIP-3,the role of necrotizing apoptosis in the development of renal IRI and the regulation of necrotizing apoptosis by HBO treatment.Methods: Our previous work has established a model of kidney transplantation in SD rats to SD rats,divided into sham operation group,renal transplantation group and renal transplantation HBO treatment group(HBO treatment group),each group was 1H,3H and5 h were divided into three groups.The renal transplantation group only underwent renal transplantation,HBO in treatment group after renal transplantation were 0h,2h and 4H in the hyperbaric oxygen treatment 1H,abdominal closure and the sham operation group only underwent right nephrectomy and without hyperbaric oxygen therapy.Kidney transplantation group and HBO treatment group respectively after 1h,3H and 5h for renal transplantation and the rats were sacrificed and the sham operation group after operation of1 H,3H and 5h after resection of the left kidney of rats.This study used paraffin blocks of project preparation of sections,the pathological changes were observed by HE staining,the expression of RIP-1,RIP-3 protein in renal tissue was detected by immunohistochemical method.Results:1.The pathological changes of kidney were observed after HE staining under the microscope: in the structure of sham operation group at each time point of the normal kidney.After renal transplantation renal tubular lumen expansion,glomerular volume,epithelial cells were swollen,some tissue showed granular degeneration,and the emergence of protein sample tube and neutrophil infiltration,with prolonged injury more serious.After HBO treatment also have different degrees of renal tubular lumen expansion,glomerular volume,epithelial cell swelling and deformation,but not the severity of renal transplantation group,only a small amount of neutrophil infiltration and granular degeneration and tissue injury in renal transplantation group.2.The changes of expression of rip-3 in rat kidney:RIP-1 and RIP-3 are mainly expressed in renal tubular epithelial cells cytoplasm,RIP-1 expression was not detected in glomeruli,glomerular expression of RIP-3 in small amount.The relative quantitative analysis showed that the expression of 1H and 3H in the transplantation group two 5h,each time point of kidney were significantly higher than those in sham operation group(P<0.05),the expression of HBO after treatment of the two significantly decreased(P<0.05),but still higher than the sham operation group(P<0.05).In renal transplantation group and HBO treatment group,with the prolongation of reperfusion time,the expression of the two gradually increased(P<0.05),with 5h reperfusion increased significantly(P<0.05);in the sham operation group,no significant difference between the expression level of each time point of the two(P>0.05).Conclusions:1.After renal transplantation appeared in the early kidney damage,significantly upregulated necroptosis key factors RIP-1 and RIP-3 in renal transplantation reperfusion can promote apoptosis,necrosis increased kidney damage,with the prolongation of reperfusion time effect is more obvious.2.After renal transplantation with HBO treatment can significantly reduce the expression of RIP-1 and RIP-3 in renal allograft,inhibit necrotic apoptosis,which play a role in renal protection.
Keywords/Search Tags:Hyperbaric oxygen, Rat, Renal transplantation, Ischemia reperfusion injury, Receptor interaction Protein kinase 1, Receptor interaction Protein kinase 3
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