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结肠粘素-2通过调节肠道平衡来减轻大鼠的急性死性胰腺炎

Zehua Huang^1,2, Huimin Wu², Junjie Fan²

¹Shanghai Key Laboratory of Pancreatic Disease, Shanghai JiaoTong University School of Medicine, Shanghai, China.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|May 30, 2023

概括

素-2 (MUC2) 在急性瘤性胰腺炎 (ANP) 中对肠道屏障功能至关重要. 在ANP模型中补充MUC2改善了肠道健康并减少了炎症,这表明其治疗潜力.

科学领域:

胃肠病学胃肠病学
细胞生物学细胞生物学
微生物学微生物学

背景情况:

素-2 (MUC2) 在肠道屏障完整性中起作用.
在急性胰腺炎 (AP) 患者中,杯状细胞功能和MUC2表达受损,与疾病严重程度相关.
在急性死性胰腺炎 (ANP) 中MUC2的特定机制尚不清楚.

研究的目的:

研究MUC2在ANP中的作用和机制.
探索MUC2补充作为ANP治疗策略的潜力.

主要方法:

使用皮洛卡尔宾诱导的ANP与MUC2耗尽和没有MUC2耗尽的老鼠模型.
分析了胰腺和结肠损伤,杯状细胞功能,肠道微生物群组成和短链脂肪酸概况.
采用TNF-α治疗的结肠杆菌来评估MUC2对炎症和紧结蛋白表达的影响.

主要成果:

MUC2的枯竭加剧了与ANP相关的损伤,杯状细胞功能障碍,肠道功能障碍和细菌转移.
补充MUC2部分扭转了这些有害影响,并改善了杯状细胞的功能.
MUC2的表达与促炎性细胞因子 (IL-1β,IL-6) 相反相关,与紧结蛋白 (Claudin 1,Occludin,ZO1) 有正相关.

结论:

在ANP期间,MUC2在维持肠道平衡中起着保护作用.
由于损害肠道屏障并促进炎症,MUC2缺乏导致ANP严重程度.
补充MUC2显示承诺作为治疗干预ANP.

关键词:

急性死性胰腺炎的发生.结肠杆菌是什么意思肠道屏障功能障碍肠道屏障功能障碍穆辛-2的使用方法短链脂肪酸短链脂肪酸

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