中文摘要：

目的观察远程缺血后适应（remote isehemia postconditioning，RIPostC）对大鼠脑缺血再灌注损伤后巨噬细胞炎症蛋白-1d（macrophage inflammatory protein，MIP-1et）表达的影响，初步探讨RIPostC对炎症反应的作用。方法采用线栓法制备MCAO模型，77只健康雄性SpragueDawley（SD）大鼠（280—310g）随机分为7组，每组11只：（1）假手术组（s）；（2）8h对照组（18）；（3）RIPostC8h组（R8）；（4）24h对照组（124）；（5）RIPostC24h组（R24）；（6）72h对照组（172）；（7）RIPostC72h组（R72）。远程缺血后适应的具体操作方法为在大鼠脑缺血即刻夹闭双侧股动脉10min，放开10min，如此共进行三个循环。分别应用荧光定量RT—PCR、免疫印迹法及免疫荧光法研究大鼠脑缺血再灌注8h、24h和72h时MIP-1etmRNA和蛋白质表达的变化。结果（1）荧光定量RT—PCR结果显示：与S组相比，I组及R组大鼠缺血后MIP-lα mRNA的表达均有所增加，其中18h、R8h和R24h组MIP-lα mRNA的表达显著升高（P〈0．05）。（2）Westernblot结果表明：与S组比较，I组及R组大鼠缺血后MIP-let蛋白水平的表达均有所增加，其中124h和172h组MIP-1α蛋白表达显著增高（P〈0．05）。与I组比较，1124h和R72h组MIP-1α蛋白表达呈下降趋势，其中R72h组下降显著，具有统计学意义（P〈0．05）。（3）免疫荧光结果显示：MIP-1α的变化趋势同Western Blot结果相同。结论MIP-lα参与了大鼠脑缺血再灌注损伤的炎症反应，而远程缺血后适应可能通过减轻炎症反应而发挥脑保护作用。

英文摘要：

Objective To observe the effect of remote ischemic postconditioning （RIPostC） on macrophage inflammatory protein-lalpha （MIP-lct） expression induced by cerebral ischemia-reperfusion injury in rats, and preliminarily explore the effect of RIPostC on int]ammatory response. Methods A total of 77 male Sprague-Dawley （SD） rats （280 -310 g） were randomly divided into7 groups： （1） Sham group （S） ; （2） ]JR 8 h group （I8） ; （3） I/R ＋ RIPostC 8 h group （RS） ; （4） I/R 24 h group （I24） ; （5） I/R ＋ RIPostC 24 h group （R24） ; （6） I/R 72 h group （I72） ; （7） I/R ＋ RIPostC 72 h group （R72）. In the I/R groups, transient middle cerel~ral artery occlusion （MCAO） models were induced. In the I/R ＋ RIPostC groups, limb RIPostC was carried out by three cycles of 10 min occlusion/10 rain release of the bilateral femoral arteries using clamps immediately after reperfusion. Real-time quantitative PCR （ QTR- PCR） , Western blot and immunofluorescence staining were used to observe the MIP-lct expression levels. Results （ 1 ） QRT-PCR demonstrated that the MIP-lot mRNA expression was increased in both I/R and I/R ＋ R groups. Among them, I8, R8 and R24 groups were significantly increased （ P 〈 0. 05 ）. （ 2 ） Western blot showed that, compared with the S group, the MIP-lct protein expression was increased in both I/R and I/R ＋ R groups. Among them, the I24 and I72 groups were significantly increased （P 〈 0. 05）. Compared with the I/R group, the MIP-lct protein expression was reduced in the R24 and R72 groups, and the R72 group was statistically significantly decreased （P 〈 0. 05 ）. （3） The immunofluorescence results were consistent with those of the Western blot. Conclusions MIP-lct is involved in the inflammatory response induced by cerebral ischemic-reperfusion injury in rats. Remote ischemic postconditioning probably reduces the inflammatory response, therefore, to play a protective role to the ischemic-reperfusion injur