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在缺血-再输液模型中分析了来自肠道微生物群的脂质代谢物
Keita Nakatsutsumi1, Koji Morishita, Todd W Costantini
1From the Trauma and Acute Critical Care Center (K.N., K.M. M.K., T.A., A.S., K.S.), Tokyo Medical and Dental University Hospital, Tokyo, Japan; Division of Trauma, Surgical Critical Care, Burns, and Acute Care Surgery, Department of Surgery (K.N., T.W.C.), University of California, San Diego, California; Department of Acute Critical Care and Disaster Medicine (M.K.), Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University; Emergency and Critical Care Center (M.K.), Tokyo Women's Medical University, Adachi Medical Center, Tokyo; Laboratory for Metabolomics (M.A.), RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa; Division of Physiological Chemistry and Metabolism (M.A.), Graduate School of Pharmaceutical Sciences, Keio University; and National Hospital Organization Disaster Medical Center (Y.O.), Tokyo, Japan.
肠道缺血会增加肠道细菌衍生的脂质,如中肠淋巴中的酸和10-基-cis-12-octadecenoic acid (HYA). 这突显了肠道微生物群和创伤后多器官功能障碍 (MOD) 之间的联系.
科学领域:
- 胃肠病学 胃肠病学
- 代谢学 代谢学 代谢学
- 创伤病理生理学
背景情况:
- 由于缺血-再输液 (IR) 损伤导致肠道屏障的破坏,导致严重创伤后多器官功能障碍 (MOD).
- 中腔淋巴 (ML) 是炎症媒介运输的关键途径,包括脂质.
- 后生物药物,如10-基-cis-12-octadecenoic acid (HYA),是潜在的治疗方法,但它们在MOD中的作用尚不清楚.
研究的目的:
- 在肠道IR大鼠模型中研究来自肠道微生物群的脂质代谢物.
- 在红外线损伤后,分析介质淋巴和血中脂质谱的变化.
主要方法:
- 雄性Sprague-Dawley大鼠经历了60分钟的上半导体动脉 (SMA) 阻塞,随后进行了120分钟的再注射.
- 在IR前和之后收集了中腔淋巴 (ML) 和血.
- 用脂质提取和液体染色学-并联质谱法 (LC-MS/MS) 来进行分析.
主要成果:
- 在IR之后,林诺酸度在ML上增加,但在血中没有增加.
- 来自肠道微生物群的10-基-cis-12-octadecenoic acid (HYA) 在ML中显示出比血更高的度.
- 在IR后ML中HYA的相对增加明显高于在血中 (3.23对0.95,p=0.048).
结论:
- 肠道IR导致ML中的林诺基酸和HYA增加,源自肠道细菌.
- 这些发现表明,肠道微生物群衍生的脂质代谢物与创伤后的MOD发展之间存在联系.
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