共刺激分子B_7 mRNA在大鼠热缺血再灌注损伤肾组织中的表达

mRNA expression of costimulatory molecular B_7 in rat renal tissue after warm ischemia/reperfusion injury

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。

Purpose:To further testify the role of costimulatory molecular B 7 in renal ischemia/reperfusion injury.Methods:The mRNA transcription level of B 7 was assayed with reverse transcription semiquantative polymerase chain reaction in the uninephrectomized rat model established by warm ischemia/reperfusion.Results:The mRNA transcription level of B 7 was very low in normal and ischemia renal tissue, but was gradually increased after repefusion,and reached peak level at 72 hours after reperfusion; The mRNA transription level of B 7 in the ischemia 60 min reperfusion group was higher than that in the ischemia 30 min reperfusion group.Conclusions:Upregulation of costimulatory molecular B 7 further elucidates the mechanism of relationship between ischemia/reperfusion injury and acute rejection; More heavier ischemia/reperfusion injury, more possible acute rejection.