肾缺血-再灌注损伤后TNF-α、IL-6和MCP-1表达变化的意义  

The significance of TNF-α,IL-6 and MCP-1 expression following renal ischemia reperfusion injury

作　　者：黄仁发[1] 周巧玲[2] 彭卫生[2] 肖洲[2] 何兰[2] 

机构地区：[1]广西中医学院附属瑞康医院肾内科,广西南宁530011 [2]中南大学湘雅医院肾内科,湖南长沙410011

出　　处：《中国现代医学杂志》2012年第21期13-17,共5页China Journal of Modern Medicine

基　　金：国家自然科学基金(No:81070552)

摘　　要：目的观察肾缺血-再灌注损伤后TNF-α、IL-6和MCP-1的表达,研究肾IR I的炎症机制。方法将健康雄性SD(Sprasue-Dawley)大鼠随机分为假手术组(sham组)和缺血-再灌注组(I/R组),通过摘除右肾,夹闭左肾蒂60 min的方法建立肾I/R大鼠模型。Sham组大鼠摘除右肾后未夹闭左肾蒂,组内分为I/R后24 h、48 h及72 h 3个时间点,分别在上述时间点处死大鼠;全自动生化仪检测两组大鼠肾功能BUN和Scr水平;ELISA法检测两组大鼠血清TNF-α、IL-6水平的变化,免疫荧光法和western blot法肾组织MCP-1蛋白的变化。结果肾IRI诱导血清BUN、Scr、TNF-α及IL-6水平显著增高,肾小管上皮细胞MCP-1蛋白表达显著上调,均于再灌注后24 h达高峰,之后逐渐下降,与sham组大鼠24 h、48 h及72 h同时间点相比较,差异均具有显著性(P<0.01)。结论肾IRI后存在炎症过程,且肾小管上皮细胞可转化为炎症细胞。【Objective】 To observe the expression of tumor necrosis factor alpha（TNF-α）,Interleukin-6（IL-6） and monocyte chemotactic protein-1（MCP-1） level,investigating the inflammation mechanism following renal ischemia/reperfusion injury.【Methods】 30 healthy male rats were divided into sham group and ischemia/reperfusion group randomly,the ischemia/reperfusion rats models were established by excising right kidneys.Subsequently,the left kidney was subjected to 60 min of ischemia with atraumatic vascular clamp,then the clamps were removed to anastate reperfusion,Sham group rats,subjected to the same surgical procedure without clamping the left renal vessels,and the rats in each group were divided into 24 h,48 h and 72 h time point respectively.The rats were sacrificed at the time points.Kidney function was evaluated by measurement of Scr and BUN level with the Biochemical Autoanalyzer,and the concentrations of serum TNF-α and IL-6 were measured by Enzyme-linked immunosorbent assay（ELISA）,the expression of MCP-1 protein in the rats kidney were detected by means of immune confocal laser microscope and western blot.【Results】 Renal ischemia/reperfusion injury induces increased level of Scr,BUN,TNF-α,and IL-6 in serum,and the expressions of MCP-1 in renal tubular following reperfusion are increased,which reached a peak at 24 h after reperfusion,decreased gradually.There are significant difference when compared to sham group rats（P 〈0.01）.【Conclusion】 Renal ischemia/reperfusion injury induces inflammation process that results to a transdifferentiation from renal epithelial Cells to inflammation cells.

关 键 词：肾缺血-再灌注损伤 炎症过程 SD大鼠 

分 类 号：R322.11[医药卫生—人体解剖和组织胚胎学] R587.1[医药卫生—基础医学]