巨噬细胞内IKKα在小鼠肾脏缺血再灌注损伤炎症反应中的作用

发布时间：2018-02-10 08:51

本文关键词： 缺血再灌注损伤炎症巨噬细胞 IKKα　出处：《南京医科大学学报(自然科学版)》2017年04期 　论文类型：期刊论文

【摘要】：目的:研究巨噬细胞内IKKα在小鼠肾脏缺血再灌注损伤(ischemic reperfusion injury,IRI)炎症反应中的作用。方法:分别将20只8~10周龄健康雄性C57BL/6小鼠(WT小鼠)、20只8~10周龄健康雄性巨噬细胞内IKKα基因敲除即IKKαMKO小鼠(KO小鼠)随机分为假手术(Sham)组和肾脏缺血再灌注损伤(IRI)组,分别构建模型。苏木素-伊红(HE)染色法观察肾脏组织形态学改变及炎症细胞浸润情况,免疫组织化学法检测肾组织抑炎因子白介素-10(IL-10)、促炎因子白介素-6(IL-6)、增殖指标Ki67、巨噬细胞标记物CD68、M1型巨噬细胞标记物诱导型一氧化氮合酶(iNOS)、M2型巨噬细胞标记物精氨酸酶1(Arg-1)的表达,Western blot检测IL-10、IL-6的表达变化。结果:HE染色结果表明IRI组较Sham组肾组织结构损伤明显及炎症浸润增加。免疫组化结果表明肾脏IRI后IL-10和IL-6均呈高表达,IL-10表达随时间延长而递增,IL-6表达随时间延长而递减。与WT-RI组相比,KO-IRI组小鼠肾脏病理损伤加重(P0.01),IL-6、CD68、iNOS表达显著增加(P0.01),IL-10(P0.01)、Ki67(P0.05)表达显著降低。结论:巨噬细胞内IKKα基因敲除加重了小鼠肾脏缺血再灌注损伤的炎症反应且不利于肾脏修复,这可能与增加了肾脏早期巨噬细胞(M1型为主)浸润及促进了炎症反应有关。
[Abstract]:Objective: to study the role of IKK 伪 in the inflammatory response of murine renal ischemia-reperfusion injury induced by ischemia reperfusion injury (IRI). Methods: 20 healthy male C57BL / 6 mice of 8 weeks old were divided into 20 healthy male macrophages at the age of 810 weeks and 20 healthy male macrophages at the age of 10 weeks. IKK 伪 knockout mice (IKK 伪 MKO mice) were randomly divided into sham-operated group and renal ischemia-reperfusion injury group. The renal histomorphology and inflammatory cell infiltration were observed by hematoxylin and eosin (HEH) staining. Detection of IL-10, IL-6, Ki67, inducible nitric oxide synthase (iNOS) and arginine, a macrophage marker CD68M1-type M _ 2 in renal tissue by immunohistochemical method. The results are as follows: (1) Immunohistochemical method for the detection of interleukin-10 (IL-10), interleukin-6 (IL-6), interleukin-6 (IL-6), the macrophage marker CD68M1-type macrophage marker, arginine (arginine). Results the expression of IL-10 and IL-6 in IRI group was significantly higher than that in Sham group, and the expression of IL-10 and IL-6 was higher in IRI group than in Sham group. Compared with the WT-RI group, the expression of IL 6 increased significantly in the KO-IRI group compared with the WT-RI group. Conclusion: the knockout of the IKK 伪 gene in macrophages aggravated the expression of IKK 伪 gene in the macrophages. The inflammatory response of renal ischemia-reperfusion injury is not conducive to renal repair. This may be associated with increased infiltration of early renal macrophage type M 1) and the promotion of inflammation.
【作者单位】：徐州医科大学研究生学院;南京医科大学附属南京医院肾内科;南京医科大学附属南京医院胸心血管外科;南京医科大学附属逸夫医院肾内科;
【基金】：国家自然科学基金(81370797)
【分类号】：R692.5

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