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目的探讨Th17细胞与肾缺血再灌注损伤的关系。方法建立小鼠肾缺血再灌注损伤模型,再灌注后不同时间点收集血清和肾脾脏标本,测定血清肌酐、PAS染色评估肾损伤情况,并计数淋巴细胞。流式细胞术检测缺血再灌注损伤过程中肾及脾脏CD4+T淋巴细胞及其亚群表达变化。结果肾缺血再灌注后6 h,肾组织损伤较轻,但淋巴细胞浸润最多。再灌注后24 h,肾组织损伤最重,然而几乎无淋巴细胞浸润。与对照组相比,缺血再灌注后小鼠脾脏及肾脏中均检测到CD4+T淋巴细胞活化,其亚群Th17细胞表达增加,而Th1和Th2细胞表达水平无变化。结论肾缺血再灌注损伤早期,淋巴细胞浸润呈现“后滞效应”。Th17细胞可能参与肾缺血再灌注损伤早期的病理过程。
Objective To investigate the relationship between Th17 cells and renal ischemia-reperfusion injury. Methods The model of renal ischemia-reperfusion injury was established in mice. Serum and kidney spleens were collected at different time points after reperfusion. Serum creatinine was measured. PAS staining was used to evaluate the renal injury. Lymphocytes were counted. Flow Cytometry to Detect the Expressions of CD4 + T Lymphocytes and Their Subsets in Renal and Spleen during Ischemic Reperfusion Injury. Results 6 h after renal ischemia / reperfusion, renal tissue injury was mild, but the most infiltrated lymphocytes. Twenty-four hours after reperfusion, the most severe renal tissue injury, but almost no lymphocytic infiltration. Compared with the control group, the activation of CD4 + T lymphocytes was detected in the spleen and kidney of mice after ischemia-reperfusion, the expression of Th17 cells was increased, while the expression of Th1 and Th2 cells was unchanged. Conclusion The early stage of renal ischemia-reperfusion injury, lymphocyte infiltration showed “delayed effect”. Th17 cells may participate in the early pathological process of renal ischemia-reperfusion injury.