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H3-R2 及其在溃疡性结肠炎中的分子通讯。

H3-R2 and Its Molecular Communication within the Context of Ulcerative Colitis.

机构信息

Key Laboratory of Dairy Science, Ministry of Education, Northeast Agricultural University, Harbin 150030, China.

Food College, Northeast Agricultural University, Harbin 150030, China.

出版信息

J Agric Food Chem. 2022 Sep 21;70(37):11678-11688. doi: 10.1021/acs.jafc.2c02909. Epub 2022 Sep 12.

DOI:10.1021/acs.jafc.2c02909
PMID:36095239
Abstract

Bifidobacteria are important mediators of immune system development within the gastrointestinal system and immunological homeostasis. The present study explored the anti-colitic activity of H3-R2 in a murine dextran sulfate sodium (DSS)-induced model of ulcerative colitis (UC). Moreover, this study offers novel insight regarding the molecular basis for the probiotic properties of H3-R2 by analyzing the underlying mechanisms whereby H3-R2-derived proteins affect the intestinal barrier. H3-R2 administration was sufficient to alleviate clinical manifestations consistent with DSS-induced colitis, restoring aberrant inflammatory cytokine production, enhancing tight junction protein expression, and positively impacting overall intestinal microecological homeostasis in these animals. Moreover, the bifidobacteria-derived GroEL and transaldolase (TAL) proteins were found to regulate tight junction protein expression via the NF-κB, myosin light chain kinase (MLCK), RhoA/Rho-associated protein kinase (ROCK), and mitogen-activated protein kinase (MAPK) signaling pathways, preventing the lipopolysaccharide (LPS)-mediated disruption of the intestinal epithelial cell barrier.

摘要

双歧杆菌是胃肠道系统中免疫系统发育和免疫稳态的重要调节者。本研究探讨了 H3-R2 在葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎(UC)小鼠模型中的抗结肠炎活性。此外,通过分析 H3-R2 衍生蛋白影响肠道屏障的潜在机制,本研究为 H3-R2 的益生菌特性提供了新的见解。H3-R2 的给药足以缓解与 DSS 诱导的结肠炎一致的临床表现,恢复异常的炎症细胞因子产生,增强紧密连接蛋白的表达,并对这些动物的整体肠道微生态平衡产生积极影响。此外,双歧杆菌衍生的 GroEL 和转醛醇酶(TAL)蛋白被发现通过 NF-κB、肌球蛋白轻链激酶(MLCK)、RhoA/Rho 相关蛋白激酶(ROCK)和丝裂原激活蛋白激酶(MAPK)信号通路调节紧密连接蛋白的表达,防止脂多糖(LPS)介导的肠上皮细胞屏障破坏。

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