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目的:研究IκB激酶α(IκB kinaseα,IKKα)对缺血再灌注(ischemia-reperfusion,IR)肾损伤恢复期小鼠炎细胞浸润及炎症介质表达的影响。方法:将C57BL/6小鼠分为假手术组、IR组、干扰组、干扰对照组。干扰组及干扰对照组提前2周给予肾实质注射慢病毒,双侧肾蒂夹闭20 min后再灌注3 d建立动物模型,假手术组仅分离肾蒂,不予夹闭。通过血肌酐、尿素氮水平和HE染色评价肾功能及组织形态学改变,免疫组织化学方法检测巨噬细胞浸润及细胞增殖情况,并通过Western blot检测IKKα、p-IKKα、肿瘤坏死因子(tumor necrosis factor,TNF)-α、白细胞介素(interleukin,IL)-18、IL-1β蛋白的表达。结果:与IR组和干扰对照组相比,IKKα干扰组血肌酐和尿素氮显著增高(P<0.05),肾组织病理损害较重,细胞增殖明显降低(P<0.05);巨噬细胞浸润及炎症介质TNF-α、IL-18、IL-1β的表达增多(P<0.05)。结论:IKKα的表达影响并且促进了肾脏缺血再灌注损伤的修复。
AIM: To investigate the effect of IκB kinase α (IκB kinase α) on inflammatory cell infiltration and inflammatory mediators in mice with convalescent of ischemia-reperfusion (IR) injury. Methods: C57BL / 6 mice were divided into sham operation group, IR group, interference group and interference control group. The interference group and the interference control group were injected with the lentivirus in the renal parenchyma two weeks in advance. After the rats were inflated with bilateral renal pedicle for 20 minutes and reperfused for 3 days, the animal model was established. The sham-operated group was only separated from the pedicel and was not clipped. The changes of renal function and histomorphology were evaluated by serum creatinine, urea nitrogen and HE staining. The infiltration of macrophages and proliferation of cells were detected by immunohistochemistry. The expressions of IKKα, p-IKKα, tumor necrosis factor, TNF) -α, interleukin (IL) -18, IL-1βprotein expression. Results: The levels of serum creatinine and urea nitrogen in IKKα interference group were significantly higher than those in IR group and control group (P <0.05). The pathological changes in renal tissue were severe and the cell proliferation was significantly decreased (P <0.05). The infiltration of macrophages and The expression of TNF-α, IL-18 and IL-1β in inflammatory mediators increased (P <0.05). Conclusion: The expression of IKKα affects and promotes the repair of renal ischemia-reperfusion injury.