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NLRP3 炎性小体在长双歧杆菌调节感染后肠易激综合征内脏敏感性中的作用。

Role of NLRP3 inflammasome in Bifidobacterium longum-regulated visceral hypersensitivity of postinfectious irritable bowel syndrome.

机构信息

a Department of Gastroenterology , The Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an , Shaanxi Province , P.R. China.

b Department of Gastroenterology , The Affiliated Hospital of Yan'an University , Yan'an , Shaanxi Province , P.R. China.

出版信息

Artif Cells Nanomed Biotechnol. 2016 Dec;44(8):1933-1937. doi: 10.3109/21691401.2015.1111238. Epub 2015 Dec 24.


DOI:10.3109/21691401.2015.1111238
PMID:26697916
Abstract

We aimed to explore the role of NLRP3 inflammasome in Bifidobacterium longum-regulated visceral hypersensitivity of postinfectious irritable bowel syndrome (PI-IBS). Fifty NIH mice were divided into five groups (n = 10). The visceral sensitivities of PI-2W and PI-8W groups significantly exceeded than those of normal control groups (P < 0.05), which was significantly decreased in PI-B group (P < 0.05). Significantly more IL-18 and IL-1β were expressed in PI-2W and PI-8W groups than those in normal control groups (P < 0.05), which was significantly decreased in PI-B group (P < 0.05). Bifidobacterium longum may down-regulate IL-18 and IL-1β expressions by inhibiting NLRP3 inflammasome and thus reduce the visceral hypersensitivity of PI-IBS.

摘要

我们旨在探讨 NLRP3 炎性体在长双歧杆菌调节肠易激综合征后感染性内脏敏感性中的作用。将 50 只 NIH 小鼠分为五组(每组 10 只)。PI-2W 和 PI-8W 组的内脏敏感性明显高于正常对照组(P<0.05),PI-B 组明显降低(P<0.05)。PI-2W 和 PI-8W 组的 IL-18 和 IL-1β 表达明显高于正常对照组(P<0.05),PI-B 组明显降低(P<0.05)。长双歧杆菌可能通过抑制 NLRP3 炎性体来下调 IL-18 和 IL-1β 的表达,从而减轻 PI-IBS 的内脏敏感性。

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