The Effect Of Uncoupling Protein-1on Ischemia-reperfusion Injury In Mice Kidney

To establish and observation the model ofkidney ischemia-reperfusion injury in C57BL/6j miceObjective:IRI model is established, a preliminary observation and evaluationabout renal damage in C57BL/6j mice and their pathological form.Methods:40 C57BL/6j mice, only satisfy experimental standards, randomly selected 30 C57 mice as damage model which is built; The remaining 10 mice as the control group. Postoperative to evaluate renal C57 mice, mice kidney injury through the kidney specimens hematoxylin eosin staining to observe, and to evaluate the level of injury:Mild, moderate, severe, finally observe operation success rate, assessment modeling method.Results:Experimental C57BL/6j mice postoperative survival rate was 93.33%, hematoxylin eosin staining showed renal tubular damage and evaluation for them into mild-to-moderate IRI damage.ConcIusion:C57BL/6j mice surgical success rate is high, the modeling method is stable and available, kidney function decline, dyeing pathological damage observed obviously and make evaluation, and completed a preliminary study of C57BL mice IRI damage.TheeffectofUncoupling protein-lonkidney ischemia-reperfusion injury inmiceObjective:Observation injury of in UCP1-defects-mice ischemia-reperfusion kidney and determine the role of UCP1.Methods:UCP1 defects in mice, male, six to eight weeks,20 to 25 g,20 as the experimental group (group UCP1), C57 mice, male, six to eight weeks,20 to 25 g, 20 as the control group (group C 57). The first part of the operation method is used to build the kidney ischemia-reperfusion injury model, after acquisition of the experimental group and control group respectively in serum and kidney specimens,.Detect the serum specimens of serum creatinine and urea nitrogen to acess the function of the kidneys.Observe the change and evaluation of renal injury.kidney pathology were observed after HE staining of kidney tissue. Determination of all specimens detect in the same time.Results:UCP1 group (168.1±36.56,36.56 ±4.81) of serum creatinine, blood urea nitrogen were higher than in control C57 group (60.99+60.99±11.16, 60.99), statistically significant differences by statistical analysis. (P< 0.001), Pathological damage is more serious which pathological UCP1 group compared with the C57 group.Conclusion:UCP1 absent increased the level of renal ischemia-reperfusion injury in mice.In other word,UCP1 protein can reduce kidney ischemia-reperfusion injury.The mechanism OF UCP1 absent in mice kidney increasing the level of IRI damageObjective:Research the mechanism of UCP1 absent in mice kidney increasing the level of IRI damage. Methods:The second part of the experimental results and the related studies showed that ROS may result in the inflammatory response which is more serious, the use of inflammatory markers of classic TNF-α to measure and evaluate the level of inflammation of kidneys, the second part of the collected specimens (80℃ refrigerator) for RT-PCR test the content of TNF-α test.Results:UCP1 group of TNF-α expression level (3.65±0.052), TNF-α C57 group expression level (1.65 ±0.048), statistically significant differences by statistical analysis. (P< 0.05)Conclusion:Defects in UCP1 TNF-α expression level in the kidney of mice significantly higher than that of C57 mice, the possible reasons for UCP1 defect group, to produce more ROS and stimulates inflammation related factor function damage the kidneys.