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目的 :观察缺血再灌注损伤对肾组织免疫原性的影响。 方法 :在大鼠单肾热缺血再灌注损伤模型的基础上 ,利用逆转录 -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、炎性细胞因子 IL - 2、TNF-α的m RNA表达水平。 结果 :正常和缺血肾组织中 B7、TNF-α、IL - 2的 m RNA表达处于极低水平 ,再灌注后肾组织中 B7、TNF-α、IL - 2的 m 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 min再灌注组的 B7、IL - 2、TNF-α的 m RNA的表达水平明显高于缺血 30 min再灌注组 (P<0 .0 5 )。 结论 :缺血再灌注损伤使共刺激分子 B7、炎性细胞因子 TNF-α、IL - 2的m RNA表达升高 ,提示缺血再灌注损伤可使移植肾免疫原性升高 ,炎症反应加强 ,这些均能促进急性排斥反应的发生
Objective: To observe the effect of ischemia-reperfusion injury on immunogenicity of kidney tissue. Methods: Based on the model of single renal reperfusion injury in rats, semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of co-stimulatory molecules B7, inflammatory cytokines IL - 2, m RNA expression of TNF-α. Results: The mRNA expressions of B7, TNF - α and IL - 2 in normal and ischemic renal tissues were extremely low. The expression of m RNA in B7, TNF - α and IL - 2 in renal tissue began to gradually increase after reperfusion , And peaked at 72 h after reperfusion. The mRNA expression levels of B7, IL - 2 and TNF - α in the reperfusion group at 60 min after ischemia were significantly higher than those at 30 min after reperfusion .0 5). CONCLUSION: The expression of costimulatory molecules B7, inflammatory cytokines TNF-α and IL-2 m RNA is increased after ischemia / reperfusion injury, suggesting that ischemia-reperfusion injury may enhance the immunogenicity and inflammatory response of renal allograft , Which can promote the occurrence of acute rejection