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目的 :进一步验证 B7- CD2 8共刺激通路在肾缺血再灌注损伤中的作用。方法 :在大鼠单肾热缺血再灌注损伤模型的基础上 ,将 6 0只雄性 SD大鼠均分为假手术组、缺血 30 min再灌注组和缺血 6 0 min再灌注组 ,利用多聚酶链反应 (RT- PCR)半定量技术检测不同损伤程度的肾组织中共刺激分子 B7的 m RNA表达水平。结果 :正常和缺血肾组织中 B7m RNA的表达处于极低水平 ,再灌注后肾组织中 B7m RNA的表达开始逐渐升高 ,并于再灌注后 72 h达高峰 ,缺血 6 0 m in再灌注组的 B7m RNA的表达水平明显高于缺血 30 min再灌注组。结论 :缺血再灌注损伤后肾组织内 B7m RNA的转录水平升高 ,进一步阐明了缺血再灌注损伤与急性排斥反应的联系机制 ;移植肾缺血再灌注损伤越重 ,发生急性排斥反应的可能性越大。
Objective: To further verify the role of B7-CD28 costimulatory pathway in renal ischemia-reperfusion injury. Methods: Sixty male Sprague-Dawley rats were randomly divided into sham operation group, 30 min ischemia reperfusion group and 60 min ischemia reperfusion group on the basis of single renal reperfusion injury model in rats. Polymerase chain reaction (RT-PCR) semi-quantitative technique was used to detect the m RNA expression level of costimulatory molecule B7 in renal tissues with different degree of injury. Results: The expression of B7mRNA in normal and ischemic renal tissues was extremely low. After reperfusion, the expression of B7mRNA began to increase in renal tissue and peaked at 72h after reperfusion, and reached the peak at 60 min The expression level of B7m RNA in the perfusion group was significantly higher than that in the reperfusion group 30min after ischemia. CONCLUSION: B7m RNA transcripts are increased in renal tissues after ischemia-reperfusion injury, which further clarifies the mechanism of ischemia-reperfusion injury and acute rejection. The more severe ischemia-reperfusion injury is, the more acute rejection occurs The greater the likelihood.