伦敦大学学院的研究团队发现了人体内一种天然的炎症关闭机制。1研究表明，环氧代谢产物分子可充当免疫系统的"天然制动器"，通过阻断溶解环氧水解酶（sEH）来增加这些分子的水平，进而有效抑制炎症反应。1这一发现为慢性炎症疾病的治疗提供了新的思路。
在人体试验中，研究人员采用了药物GSK2256294进行测试。1预防性给药组在炎症开始前2小时给药，包括12名治疗组和12名安慰剂对照组志愿者；治疗性给药组则在炎症开始后4小时给药，同样包括各12名参与者。1试验结果显示，该药物能够加速疼痛缓解，并显著减少血液和组织中的中间单核细胞数量。1
研究进一步揭示了作用机制：环氧代谢产物12,13-EpOME可以抑制p38 MAPK蛋白信号通路。1这项研究已发表在《自然通讯》期刊，由关节炎英国基金会资助，涉及伦敦大学学院、伦敦国王学院、牛津大学、伦敦玛丽女王大学和美国国家环境健康科学研究所等多家机构的合作。1
Researchers at University College London have identified a biological mechanism that halts inflammatory responses through molecules called epoxide metabolites, which act as a natural brake on the immune system.1 In human trials, increasing these molecules by blocking soluble epoxide hydrolase (sEH) accelerated pain relief and substantially reduced intermediate monocytes that can trigger chronic inflammation, offering a new therapeutic pathway for inflammatory diseases.1
The study, published in Nature Communications on September 12, 2026, tested the drug GSK2256294, which works by inhibiting sEH to elevate epoxide metabolite levels.1 Two groups of 24 volunteers each participated: a preventive group receiving the treatment two hours before inflammation onset, and a therapeutic group treated four hours after inflammation began.1 Both approaches demonstrated faster pain relief, with intermediate monocyte counts declining significantly in blood and tissue samples.1 The research revealed that the specific epoxide metabolite 12,13-EpOME suppresses the p38 MAPK protein signaling pathway, a key driver of inflammatory responses.1
The work involved collaboration among University College London, King's College London, University of Oxford, Queen Mary University of London, and the U.S. National Institute of Environmental Health Sciences, with funding from Arthritis UK.1
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