Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway
作者机构:Department of AnesthesiologyThe First Affiliated Hospital of Zhejiang Chinese Medical University(Zhejiang Provincial Hospital of Traditional Chinese Medicine)Hangzhou 310006Zhejiang ProvinceChina Department of EmergencyXinhua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200092China
出 版 物:《World Journal of Diabetes》 (世界糖尿病杂志(英文版)(电子版))
年 卷 期:2024年第15卷第9期
页 面:1962-1978页
核心收录:
学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
主 题:Diabetes Dexmedetomidine Intestinal barrier Piezo1 Tight junctions
摘 要:BACKGROUND Diabetes is often associated with gastrointestinal dysfunctions,which can lead to ***(DEX)is a commonly used sedative in perioperative diabetic patients and may affect gastrointestinal *** To investigate whether sedative doses of DEX alleviate diabetes-caused intestinal *** Sedation/anesthesia scores and vital signs of streptozotocin(STZ)-induced diabetic mice under DEX sedation were *** mice were divided into saline and DEX *** injecting sedatives intraperitoneally,tight junctions(TJs)and apoptotic levels were evaluated 24 hours later to assess the intestinal barrier *** role of DEX was validated using Villin-MMP23B flox/flox mice with intestinal epithelial *** vitro,high glucose and hyperosmolarity were used to culture Caco-2 monolayer cells with STZ *** techniques were used to monitor the barrier and mitochondrial *** MMP23B protein levels in the intestinal tissue of STZ-induced diabetic mice were significantly higher than those in the intestinal tissue of control mice,with the DEX group displaying decreased MMP23B ***-mediated TJ disruption,increased intestinal mucosal permeability,and systemic inflammation in wild-type mice might be reversed by *** Caco-2 cells,MMP23B was associated with increased reactive oxygen species accumulation,mitochondrial membrane potential depolarization,and TJ *** DEX reduces MMP23B,which may potentially contribute to STZ-induced intestinal barrier dysfunction,affecting TJ modification through mitochondrial dysfunction.