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The Protection Of Protein Kinase C Beta Inhibitors On Renal Ischemia-reperfusion Injury By Influencing Macrophage Subtypes

Posted on:2018-10-16Degree:MasterType:Thesis
Country:ChinaCandidate:T XiaoFull Text:PDF
GTID:2334330536958398Subject:Renal medicine
Abstract/Summary:PDF Full Text Request
Objective: To investigate the effect of protein kinase C ?(PKC?)inhibitor on inflammatory mediators in renal ischemia-reperfusion injury by establishing the renal ischemia-reperfusion injury model through gavage of PKC? inhibitor,in order to explore the protective mechanism of PKC? inhibitor on renal ischemia-reperfusion injury.Methods: Renal ischemia-reperfusion injury model in rats were made and divided into three groups: renal ischemia-reperfusion injury model group(group A),renal ischemia-reperfusion injury with PKC beta inhibitor treatment group(group B)and control group(group C),In A group rats the right kidney was removed,then the left kidney was reperfused 24 hours after ischemia for 60 min according to conventional methods(the kidney pedicle was clamped);in Group B preoperative intervention via oral gavage PKC beta inhibitor was given;in Group C rats were only operated with opening and closing the abdomen.24 hours later we collect the inferior vena venous blood and kidney specimens for testing: 1.with automatic biochemical analyzer serum creatinine and urea nitrogen level were analyzed;2.PAS staining was performed to observe the renal pathological tissue damage degree;3.with immunhistochemical method to detect the expression of kidney injury molecule-1,renal papillary antigen-1and arginase-1,induced nitric oxide synthase-1.Results: 1.With the automatic biochemical analyzer the levels of serum creatinine and urea levels showed: the group A and group B are significantly increased compared with group C(P<0.01);and contrast with group B,the serum creatinine levels of group A is decreased(P<0.01),but the urea levels has no obvious change(P>0.05).2.Renal tissue PAS staining: in the group A renal tubules is seriously damaged and disorder,renal interstitial edema and inflammatory cell has infiltrated,renal tubular gap was increased,lumen expansion,renal tubular brush border loss,tubular epithelial cells were flat,visible off,and a large number of casts;renal tubular structure of group B is clearer than group A,renal interstitial edema and inflammatory cell infiltration was reduced,the renal tubule brush border was intact,tubular epithelial cell was swelling,degeneration,occasionally shedding or cast;group C The structure was clear,the basement membrane was complete,no interstitial edema,but inflammatory cell infiltration were seldom found;3.Immunohistochemistry showed that the expression of KIM-1 and RPA-1 in the group C is very few,the group A and group B significantly more than group C(P<0.01);also the group A has greater than group B(P<0.01);there is a similar results of induced nitric oxide synthase-1;However the results of arginase-1 is that the expression of group B significantly more than group A and C(P<0.01),and the rats of group B express more than group C(P<0.01).Conclusion: PKC beta inhibitor has protective effect on renal ischemia-reperfusion injury through influencing macrophage subtype cells.
Keywords/Search Tags:Macrophage, Protein kinase C inhibitors, Renal ischemia-reperfusion injury
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