小肠缺血再灌注（II/R）损伤是临床常见的组织器官损伤之一，可并发严重的全身炎症反应综合征（SIRS）和多器官功能障碍综合征（MODS），具有较高的死亡率。近年研究发现，氧化应激损伤和细胞凋亡是II/R时肠黏膜屏障破坏的主要病理基础。我们前期研究证实：双功能抗氧化酶Peroxiredoxin6（PRDX6）在II/R损伤的小肠组织中表达降低，提示肠道损伤与PRDX6的缺乏密切相关；而应用沉默信息调节因子1（SIRT1）激动剂能显著升高II/R大鼠小肠组织中PRDX6水平，并改善肠黏膜组织病理表现。据此，我们提出SIRT1通过调控PRDX6保护肠黏膜上皮细胞抵御II/R诱导的氧化应激损伤的假说。本研究在此基础上，进一步构建SIRT1基因干扰及过表达大鼠，采用先进分子生物学技术，探索II/R过程中SIRT1对PRDX6的作用及调控机制，为II/R肠黏膜屏障损伤的防治提供新的研究思路和干预策略。

Intestinal ischemia reperfusion (II/R) injury is one of the tissue and organ damage which commonly occurrs in clinic, and it may be complicated by severe systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), with higher mortality rate. Recent studies have found that oxidative stress and apoptosis are the main pathological basis of the II/R intestinal mucosal barrier disruption. Our previous studies have demonstrated that antioxidant enzymes Peroxiredoxin6 (PRDX6)’s expression decreased in II/R injury, which means intestinal injury is closely related with the lack of PRDX6. However, the application of sirtuin 1 (SIRT1) agonists in II/R significantly increases PRDX6 level compared with II/R group, and protects against intestinal mucosa injury. Accordingly, we point out that SIRT1 may protect intestinal epithelial cells against oxidative stress by regulating the expression of PRDX6. Based on the above experiment, we plan to use SIRT1 gene interference and overexpression model of rats to investigate the role of SIRT1 on PRDX6’s regulatory mechanisms in II/R process, and a variety of advanced molecular biology techniques will be used. Moreover, we also focus on the new ideas and intervention strategies for prevention and treatment of intestinal mucosal barrier disruption induced by II/R injury.