IL-17在小鼠肾脏缺血再灌注损伤表达的变化及意义

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目的:观察小鼠肾脏缺血再灌注损伤(IR)后不同时间点的血清及肾组织中白细胞介素-17(IL-17)的变化情况。方法:将C57BL/6雄性小鼠随机分为两组。假手术组(n=20)小鼠仅暴露腹腔游离肾蒂,30分钟后关闭腹腔;IR组(n=20)采用100g压力无创血管夹夹闭双侧肾蒂,30分钟后去除,恢复血流。于肾脏IR手术再灌注后3、6、12、24小时收集小鼠血浆及肾脏标本,用全自动生化仪分析血清中肌酐(SCr)与尿素氮(BUN)含量;用HE染色法观察小鼠肾脏组织病理变化;应用酶联免疫吸附法(ELISA)检测不同时间点小鼠血清及肾脏组织中IL-17的含量。结果:肾脏IR诱导小鼠血清BUN、SCr水平显著增高,肾小管坏死率也显著增加,均于IR后24小时达高峰,与假手术组小鼠3、6、12及24小时同时间点相比较,差异有统计学意义(P<0.01);小鼠血清及肾组织中IL-17含量也随病情进展表现出升高趋势,IR后24小时达顶峰,与假手术组同时间点相比,差异均具有统计学意义(P<0.01)。结论:小鼠肾IR后血清及肾组织中IL-17表达明显增加,大量IL-17表达与肾IR后炎症反应的发生密切相关。IL-17的大量表达可能对小鼠肾脏功能损伤及病理改变有诱导或促进作用。 Objective: To observe the changes of interleukin-17 (IL-17) in serum and kidney tissue of kidney after ischemia-reperfusion (IR) in mice. Methods: C57BL / 6 male mice were randomly divided into two groups. The sham operation group (n = 20) mice were exposed only to the peritoneal free renal pedicle and the abdominal cavity was closed after 30 minutes. The IR group (n = 20) was occluded with 100g pressure noninvasive vascular clamp to remove the bilateral renal pedicle. After 30 minutes, flow. Plasma and kidney samples were collected at 3, 6, 12, and 24 hours after reperfusion of renal IR. Serum creatinine (SCr) and urea nitrogen (BUN) were detected by automatic biochemical analyzer. The histopathological changes of kidney were observed. The levels of IL-17 in serum and kidneys of mice at different time points were detected by enzyme-linked immunosorbent assay (ELISA). Results: The serum levels of BUN and SCr in renal IR-induced mice were significantly increased, and the necrosis of renal tubules was also significantly increased, both of which peaked at 24 hours after IR. Compared with the sham-operated mice at 3, 6, 12 and 24 hours, (P <0.01). The content of IL-17 in the serum and kidney tissue of mice also showed an increasing trend with the progress of the disease, reaching the peak at 24 hours after IR, compared with the sham operation group at the same time point , The differences were statistically significant (P <0.01). CONCLUSION: The expression of IL-17 in serum and kidney of mice with renal IR increased significantly, and a large number of IL-17 expression was closely related to the occurrence of inflammation after renal IR. The overexpression of IL-17 may induce or promote the renal dysfunction and pathological changes in mice.
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