Cai Yujing, Wu Yanan, Guo Zhimin, Ye Yingxian, Zhu Yi, Wen Lanqi, Li Haifeng, Han Xue, Chen Daili, Duan Xuefei
Department of Anesthesiology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong Province, China.
Department of Anesthesiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, China.
Med Gas Res. 2025 Sep 1;15(3):398-403. doi: 10.4103/mgr.MEDGASRES-D-24-00033. Epub 2025 Feb 8.
Sevoflurane is a widely used inhalation anesthetic during the perioperative period. Recent studies have suggested that sevoflurane has an enteroprotective effect, but its mechanism is unclear. To explore the mechanism of sevoflurane in intestinal ischemia‒reperfusion injury, an intestinal ischemia‒reperfusion injury mouse model was established. First, intestinal ischemia‒reperfusion injury was compared between aged and young mice. The results showed that intestinal ischemia‒reperfusion injury caused pathological intestinal injury and disrupted the intestinal mucosal barrier. The aged mice had more severe intestinal ischemia‒reperfusion injury than the young mice and therefore had a lower survival rate. The aged mice subsequently received sevoflurane via inhalation. Sevoflurane alleviated the pathological injury to the intestinal mucosa and repaired the function of the intestinal mucosal barrier in aged mice, thus increasing the level of intestinal mucosal hypoxia-inducible factor-1α and improving the survival rate of aged mice. However, preoperative administration of the hypoxia-inducible factor-1α inhibitor BAY87-2243 could counteract the enteroprotective effect of sevoflurane and lower the expression level of heme oxygenase-1, a downstream antioxidant enzyme of hypoxia-inducible factor-1α. Our findings suggest that sevoflurane alleviates intestinal ischemia‒reperfusion injury in aged mice by repairing the intestinal mucosal barrier through the activation of hypoxia-inducible factor-1α/heme oxygenase-1, providing a new target for the treatment of intestinal ischemia‒reperfusion injury in aged mice.
七氟醚是围手术期广泛使用的吸入性麻醉剂。最近的研究表明，七氟醚具有肠保护作用，但其机制尚不清楚。为了探究七氟醚在肠缺血-再灌注损伤中的作用机制，建立了肠缺血-再灌注损伤小鼠模型。首先，比较了老年和年轻小鼠的肠缺血-再灌注损伤情况。结果显示，肠缺血-再灌注损伤导致肠道病理损伤并破坏肠黏膜屏障。老年小鼠的肠缺血-再灌注损伤比年轻小鼠更严重，因此存活率更低。随后，老年小鼠通过吸入方式给予七氟醚。七氟醚减轻了老年小鼠肠黏膜的病理损伤，修复了肠黏膜屏障功能，从而提高了肠黏膜缺氧诱导因子-1α水平，提高了老年小鼠的存活率。然而，术前给予缺氧诱导因子-1α抑制剂BAY87-2243可抵消七氟醚的肠保护作用，并降低缺氧诱导因子-1α下游抗氧化酶血红素加氧酶-1的表达水平。我们的研究结果表明，七氟醚通过激活缺氧诱导因子-1α/血红素加氧酶-1修复肠黏膜屏障，从而减轻老年小鼠的肠缺血-再灌注损伤，为老年小鼠肠缺血-再灌注损伤的治疗提供了新的靶点。
