青年和老年小鼠脑缺血再灌注心肺损伤的机制

发布时间：2018-05-31 10:18

本文选题：脑卒中后并发症 + 大脑中动脉栓塞模型　；参考：《细胞与分子免疫学杂志》2017年06期

【摘要】：目的研究小鼠脑缺血再灌注心肺组织损伤情况及机制。方法按5~6月龄和20~21月龄,将C57BL/6J小鼠分为青年和老年组。实验组设立假手术组,模型组为缺血1 h再灌注1、12、24、48 h组。取各灌注时间点的小鼠心肺组织,HE和TUNEL染色观察形态学改变,化学比色法检测心脏Na~+-K~+-ATP酶、Ca~(2+)-ATP酶变化,称重法计算肺指数,Western blot法分别检测心肺组织中核因子κBp65(NF-κBp65)、磷酸化NF-κBp65(p-NF-κBp65)、核因子κB抑制蛋白α(IκBα)、磷酸化IκBα(p-IκBα)水平,ELISA检测白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)水平,比色法测定一氧化氮(NO)水平。结果青年和老年小鼠分别在再灌注24 h和再灌注1 h发生肺部炎症反应,而分别于再灌注24 h和再灌注12 h可见心脏出血,肺对再灌注刺激的反应比心脏组织更早。同时在对Na~+-K~+-ATP酶、Ca~(2+)-ATP酶、肺指数、NF-κB信号通路与炎症因子的测定发现,这些指标在青年和老年小鼠组上的变化与其病理组织变化时程一致。结论老年小鼠脑缺血再灌注后会引起心肺组织的损伤,能量代谢和炎症级联反应为其损伤的主要机制。
[Abstract]:Objective to study the mechanism of cardiopulmonary injury after cerebral ischemia reperfusion in mice. Methods C57BL/6J mice were divided into two groups according to the age of 5 ~ 6 months and 20 ~ 21 months old. Sham operation group was established in the experimental group. The model group was treated with ischemia for 1 h and reperfusion for 48 h. The morphological changes were observed by HE and TUNEL staining in heart and lung tissues of mice at different perfusion time points, and the changes of Na ~ -K ~ -ATPase 2 + -ATPase in heart were detected by chemical colorimetry. The levels of nuclear factor 魏 B p65 NF- 魏 B p65, phosphorylated NF- 魏 B p65 p-NF- 魏 Bp65, nuclear factor- 魏 B inhibitor 伪 -I 魏 B 伪, phosphorylated I 魏 B 伪 -p-I 魏 B 伪, phosphorylated I 魏 B 伪 -p-I 魏 B 伪), interleukin 1 尾 -1 尾 -1 尾, tumor necrosis factor 伪 -TNF- 伪) in heart and lung tissues were measured by blot method. The levels of nitric oxide (no) were determined by colorimetric method. Results Pulmonary inflammation occurred in young and aged mice at 24 h and 1 h of reperfusion, respectively, but cardiac hemorrhage was observed at 24 h and 12 h of reperfusion, respectively. The response of lung to reperfusion stimulation was earlier than that of heart tissue. At the same time, it was found that the changes of Na ~ -K ~ -ATPase, pulmonary index and NF- 魏 B signaling pathway and inflammatory factors in young and aged mice were consistent with the time course of pathological changes. Conclusion brain ischemia and reperfusion can induce cardiopulmonary injury in aged mice. Energy metabolism and inflammatory cascade are the main mechanisms of injury.
【作者单位】：南昌大学第一附属医院药学部;南昌大学转化医学研究院心血管疾病研究中心;
【基金】：江西省卫生计生委科技计划项目(20175081)
【分类号】：R743.3

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