FK506对大鼠缺血再灌注肾细胞间黏附分子-1，p38丝裂原活化蛋白激酶表达的影响

Effect of FKS06 on ICAM-1 ,p38MAPK protein expression in renal ischemia-reperfusion injury in rats

目的探讨FK506对肾缺血再灌注不同时间细胞问黏附分子-1（ICAM-1），p38丝裂原活化蛋白激酶（p38MAPK）蛋白表达的影响。方法采用HE染色分析缺血再灌注肾组织病理损伤程度，免疫组织化学二步法检测缺血再灌注肾不同时间ICAM-1，p38MAPK蛋白表达的变化。结果ICAM-1蛋白以在肾血管表达为著。缺血45min，再灌注2h有少量表达（11．52±0．45），再灌注6、12h呈阳性表达，直至24h仍有增高趋势（加．54±1．17），FK506＋IR组肾组织ICAM-1蛋白水平显著低于IR组（P〈0．05）。p38MAPK蛋白主要在远曲小管上皮细胞表达，缺血45min，再灌注2h有少最表达（25．25±1．97），再灌注6、12h及24h呈阳性表达，6h达高峰（42．03±1．85），FK506＋IR组肾组织p38MAPK蛋白水平显著低于lR组（P〈0．01）。苏木索-伊红（HE）染色可见1R组肾小管上皮细胞有不同程度的片状坏死灶和炎性细胞浸润，FK506＋IR组肾组织损伤明显减轻。结论FK506可能通过下调ICAM-1，p38MAPK蛋白表达水平，减轻肾缺血再灌注损伤。

Objective To investigate the effect of FKS06 on ICAM-1, p38MAPK protein expression at different ischemia-reperfusion points. Methods Pathomorphological changes of renal ischemiareperfusion injury were observed by HE stain and two-step immunohistochemical methods were used to dedect the changes of expression of ICAM- I , p38MAPK. Results ICAM-1 mainly expressed in renal veins ,gradually upregulated with duration of ischemia-reperfusion to 24 h of reperfusion （20.54 ± 1.17）, but these effects were offset by administration of FK506 （P 〈 0.05 ）. p38MAPK mainly located at distal convoluted tubules ,peaked at 6 h of reperfusion （42.03 ± 1.85 ） and was decreased significantly by injection of FK506 （P 〈 0.01 ）. In IR group local necrosis and inflammatory cell infiltration were found by HE stain, while similar changes were scarcely visible in FK506 ＋ IR group. Conelusion Renal ischemiareperfusion injury can be alleviated by FK506 treatment.