Intestinal ischemia/reperfusion (I/R)-induced injury is an inflammatory response with significant morbidity and mortality. The early inflammatory response includes neutrophil infiltration. However, the majority of rodent studies utilize male mice despite a sexual dimorphism in intestinal I/R-related diseases. We hypothesized that sex may alter inflammation by changing neutrophil infiltration and eicosanoid production. To test this hypothesis, male and female C57Bl/6 mice were subjected to sham treatment or 30 min intestinal ischemia followed by a time course of reperfusion. We demonstrate that compared to male mice, females sustain significantly less intestinal I/R-induced tissue damage and produced significant LTB₄ concentrations. Male mice release PGE₂. Finally, treatment with a COX-2 specific inhibitor, NS-398, attenuated I/R-induced injury, total peroxidase level, and PGE₂ production in males, but not in similarly treated female mice. Thus, I/R-induced eicosanoid production and neutrophil infiltration varies between sexes suggesting that distinct therapeutic intervention may be needed in clinical ischemic diseases.

肠道缺血/再灌注 (I/R) 诱导的损伤是一种具有显着发病率和死亡率的炎症反应。早期炎症反应包括中性粒细胞浸润。然而，尽管肠道 I/R 相关疾病存在性别二态性，但大多数啮齿动物研究使用雄性小鼠。我们假设性别可能通过改变中性粒细胞浸润和类二十烷酸的产生来改变炎症。为了验证这一假设，雄性和雌性 C57Bl/6 小鼠接受了假治疗或 30 分钟的肠道缺血，然后是再灌注的时间过程。我们证明，与雄性小鼠相比，雌性小鼠承受的肠道 I/R 诱导的组织损伤显着减少，并产生显着的 LTB ₄浓度。雄性小鼠释放 PGE ₂. 最后，用 COX-2 特异性抑制剂 NS-398 治疗可减轻雄性I/R 诱导的损伤、总过氧化物酶水平和 PGE ₂产生，但在类似处理的雌性小鼠中则不然。因此，I/R 诱导的类二十烷酸产生和中性粒细胞浸润因性别而异，这表明在临床缺血性疾病中可能需要不同的治疗干预。