中文摘要：

目的探讨地塞米松对小鼠小肠缺血-再灌注损伤的作用及其机制。方法健康雄性C57BL/6小鼠18只,随机分为3组（n=6）,分别为假手术组、模型对照组和地塞米松组。假手术组和模型对照组缺血前30 min腹腔注射0.9%氯化钠溶液,地塞米松组缺血前30 min腹腔注射地塞米松10 mg·kg^-1,模型对照组和地塞米松组小鼠用血管夹夹闭肠系膜上动脉,置于32℃温箱30 min后松开血管夹。再灌注24 h后处死小鼠,收集血清和小肠标本。苏木精-伊红染色后观察小肠黏膜病理形态学变化并进行损伤评分,聚合酶链反应（PCR）检测白细胞介素6（IL-6）、干扰素（IFN-γ）和肿瘤坏死因子（TNF-α）,Western blotting检测p-AKT和AKT。结果假手术组、模型对照组和地塞米松组小肠损伤评分分别为（4±2）,（13±3）,（7±2）分。模型对照组IL-6、IFN-γ和TNF-αmRNA水平明显上调,p-AKT表达明显增加。与模型对照组比较,地塞米松组小肠损伤评分下降,IL-6、IFN-γ和TNF-α表达降低,p-AKT表达进一步增加。结论地塞米松预处理可通过激活AKT信号通路抑制炎症反应,从而减轻小肠缺血-再灌注损伤。

英文摘要：

Objective To investigate potential effect and mechanism of dexamethasone （ DEX） on intestinal ischemia reperfusion injury. Methods A total of 18 male C57BL/6 mice were randomly divided into three groups（ n=6 each）： sham operation group, model control group , and DEX group. Mice in the model control and sham operation groups received intraperitoneal normal saline 0. 5 hour before ischemia, and mice in DEX group received intraperitoneal injection of DEX 10 mg·kg^-1 , 0. 5 hour before ischemia. Mice in the model control and DEX groups were placed in the 32 degree infant incubator for 30 minutes after clamping superior mesenteric artery, followed by clamps removal and reperfusion for 24 hours. Mice were then sacrificed to obtain the intestinal tissues. The pathology of intestinal tissues was observed after hematoxylin-eosinstaining （ HE） staining. The mRNA expression level of pro-inflammatory cytokines IL-6, TNF-α and IFN-γ were measured by PCR. The expression of AKT and p-AKT were measured by Western blotting. Results The level of mesenteric injuries in the sham operation group, model control group and DEX group was （4±2）,（13±3）,（7±2） points, respectively. The mRNA level of IL-6, TNF-α and IFN-γ and the expression of p-AKT were all higher in the model control group. Compared to the model control group, the level of mesenteric injuries, the mRNA level of IL-6, TNF-αand IFN-γin DEX group were significantly attenuated, but the expression of p-AKT were further increased. Conclusion Pretreatment with DEX can reduce intestinal ischemia-reperfusion injury by activating AKT signaling pathway and suppressing inflammation.