Wu Yue, Liu Yan, Liu Yiping, Liu Zhiling, Yao Jiaqi, Wen Qingping
Department of Anesthesiology, The First Affiliated Hospital of Dalian Medical University, Dalian, 116011, China.
BMC Pharmacol Toxicol. 2025 Jul 26;26(1):137. doi: 10.1186/s40360-025-00975-3.
Severe abdominal pain and multiple organ dysfunction are the hallmarks of acute pancreatitis (AP). Opioid medications are effective in alleviating AP patients' pain; however, they may exacerbate the severity of the condition.
This study investigated the potential of bone marrow mesenchymal stem cell-derived small extracellular vesicles (BMSC-sEVs) to inhibit the aggravation effect of opioids through the dual mechanism of gut microbiome-immune crosstalk through data mining and in vivo experiments.
Genetic evidence suggests that opioid exposure is linked to gut microbiome dysbiosis, excessive inflammation, and susceptibility to AP. In the rat model, the inflammatory cell infiltration and pancreatic necrosis were exacerbated by the continuously increasing dose of morphine, while these effects were mitigated by antibiotic-driven microbial exhaustion. The primary point is that BMSC-sEVs has the potential to rectify the pancreatic injury that has been exacerbated by morphine by restoring the equilibrium of Bacteroidetes/Pleurophyla and inhibiting CCL3-mediated inflammation.
The gut microbiome-immune axis is the primary factor contributing to the aggravation of AP caused by opioids. BMSC-sEVs can be positioned as a novel drug for the treatment of AP, as it effectively regulates gut microbiome-immune crosstalk to coordinate analgesia and inflammation.
严重腹痛和多器官功能障碍是急性胰腺炎(AP)的特征。阿片类药物可有效缓解AP患者的疼痛;然而,它们可能会加重病情的严重程度。
本研究通过数据挖掘和体内实验,研究了骨髓间充质干细胞衍生的小细胞外囊泡(BMSC-sEVs)通过肠道微生物群-免疫串扰的双重机制抑制阿片类药物加重作用的潜力。
基因证据表明,接触阿片类药物与肠道微生物群失调、过度炎症和对AP的易感性有关。在大鼠模型中,不断增加剂量的吗啡会加剧炎症细胞浸润和胰腺坏死,而抗生素驱动的微生物耗竭可减轻这些影响。关键在于,BMSC-sEVs有可能通过恢复拟杆菌门/厚壁菌门的平衡并抑制CCL3介导的炎症来纠正由吗啡加剧的胰腺损伤。
肠道微生物群-免疫轴是导致阿片类药物加重AP的主要因素。BMSC-sEVs可被定位为一种治疗AP的新型药物,因为它能有效调节肠道微生物群-免疫串扰,以协调镇痛和炎症反应。