Cheng Ming-Zhen, Luo Jia-Hao, Li Xin, Liu Feng-Yong, Zhou Wei-Jie
State Key Laboratory of Organ Failure Research, Department of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China.
Department of Interventional Radiology, The Fifth Medical Centre, Chinese PLA General Hospital, Beijing 100071, China.
World J Gastrointest Surg. 2024 Dec 27;16(12):3843-3856. doi: 10.4240/wjgs.v16.i12.3843.
Intestinal ischemiareperfusion (I/R) injury (II/RI) is a critical condition that results in oxidative stress, inflammation, and damage to multiple organs. Zinc, an essential trace element, offers protective benefits in several tissues during I/R injury, but its effects on intestinal II/RI remain unclear.
To investigate the effects of zinc pretreatment on II/RI and associated multiorgan damage.
C57BL/6 mice were pretreated with zinc sulfate (ZnSO, 10 mg/kg) daily for three days before I/R injury was induced superior mesenteric artery occlusion (SMAO) and abdominal aortic occlusion (AAO) models. Tissue and serum samples were collected to evaluate intestinal, liver, and kidney damage using Chiu's score, Suzuki score, and histopathological analysis. Caco-2 cells and intestinal organoids were used for hypoxiareoxygenation injury models to measure reactive oxygen species (ROS) and superoxide dismutase (SOD) levels.
Zinc pretreatment significantly reduced intestinal damage in the SMAO and AAO models ( < 0.001). The serum levels of liver enzymes (alanine aminotransferase, aspartate aminotransferase) and kidney markers (creatinine and urea) were lower in the zinc-treated mice than in the control mice, indicating reduced hepatic and renal injury. , zinc decreased ROS levels and increased SOD activity in Caco-2 cells subject to hypoxiareoxygenation injury. Intestinal organoids pretreated with zinc exhibited enhanced resilience to hypoxic injury compared to controls.
Zinc pretreatment mitigates II/RI and reduces associated multiorgan damage. These findings suggest that zinc has potential clinical applications in protecting against I/R injuries.
肠道缺血再灌注（I/R）损伤（II/RI）是一种危急情况，可导致氧化应激、炎症反应以及多器官损伤。锌作为一种必需的微量元素，在I/R损伤期间对多个组织具有保护作用，但其对肠道II/RI的影响尚不清楚。
研究锌预处理对II/RI及相关多器官损伤的影响。
在通过肠系膜上动脉闭塞（SMAO）和腹主动脉闭塞（AAO）模型诱导I/R损伤前三天，每天给C57BL/6小鼠腹腔注射硫酸锌（ZnSO₄，10mg/kg）。采集组织和血清样本，使用Chiu评分、Suzuki评分和组织病理学分析评估肠道、肝脏和肾脏损伤情况。使用Caco-2细胞和肠道类器官构建缺氧复氧损伤模型，检测活性氧（ROS）和超氧化物歧化酶（SOD）水平。
锌预处理显著减轻了SMAO和AAO模型中的肠道损伤（P<0.001）。锌处理组小鼠的血清肝酶（丙氨酸转氨酶、天冬氨酸转氨酶）和肾脏标志物（肌酐和尿素）水平低于对照组小鼠，表明肝损伤和肾损伤减轻。此外，锌降低了缺氧复氧损伤的Caco-2细胞中的ROS水平，并增加了SOD活性。与对照组相比，锌预处理的肠道类器官对缺氧损伤的耐受性增强。
锌预处理可减轻II/RI并减少相关的多器官损伤。这些研究结果表明，锌在预防I/R损伤方面具有潜在的临床应用价值。
