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多糖诱导的肠道紧密连接损伤缓解:在小鼠内毒素血症模型中对NF-κB/MLCK途径的抑制

polysaccharides-induced intestinal tight junction injury alleviation inhibition of NF-κB/MLCK pathway in a mouse endotoxemia model.

作者信息

Han Jie, Li Ji-Hong, Bai Guang, Shen Guo-Shun, Chen Jing, Liu Jia-Nan, Wang Shuo, Liu Xian-Jun

机构信息

Jie Han, Guo-Shun Shen, Jing Chen, Jia-Nan Liu, Xian-Jun Liu, Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, Liaoning Province, China.

出版信息

World J Gastroenterol. 2017 Mar 28;23(12):2175-2184. doi: 10.3748/wjg.v23.i12.2175.

DOI:10.3748/wjg.v23.i12.2175
PMID:28405145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5374129/
Abstract

AIM

To examine the effects of polysaccharides (ASPS) on intestinal tight junction (TJ) disruption and nuclear factor-kappa B (NF-κB)/myosin light chain kinase (MLCK) activation in endotoxemia.

METHODS

BALB/C mice (6-8-weeks-old) received continuous intragastric gavage of ASPS for 7 d before injection of lipopolysaccharide (LPS), or received ASPS once after LPS injection. Blood and intestinal mucosal samples were collected 6 h after LPS challenge. Clinical symptoms, histological injury, intestinal permeability, TJ ultrastructure, and TJ protein expression were determined.

RESULTS

Compared with mice in the LPS group, pretreatment with ASPS improved clinical and histological scores by 390.9% ( < 0.05) and 57.89% ( < 0.05), respectively, and gut permeability change in endotoxemic mice was shown by a 61.93% reduction in reduced leakage of fluorescein isothiocyanate-dextran 6 h after LPS injection ( < 0.05). ASPS pretreatment also prevented LPS-induced TJ ultrastructure breakdown supported by increased electron dense materials between adjoining cells, sustained redistribution and expression of occludin (0.597 ± 0.027 0.103 ± 0.009, < 0.05) and zonula occludens-1 (0.507 ± 0.032 0.125 ± 0.019, < 0.05), and suppressed activation of the NF-κB/MLCK pathway indicated by reduced expression of NF-κB, phospho-inhibitor kappa B-alpha, MLCK and phospho-myosin light-chain-2 by 16.06% ( < 0.05), 54.31% ( < 0.05), 66.10% ( < 0.05) and 64.82% ( < 0.05), respectively.

CONCLUSION

ASPS pretreatment may be associated with inhibition of the NF-κB/MLCK pathway and concomitant amelioration of LPS-induced TJ dysfunction of intestinal epithelium in endotoxemia.

摘要

目的

研究多糖(ASPS)对内毒素血症小鼠肠道紧密连接(TJ)破坏及核因子-κB(NF-κB)/肌球蛋白轻链激酶(MLCK)激活的影响。

方法

6至8周龄的BALB/C小鼠在注射脂多糖(LPS)前连续7天接受ASPS灌胃,或在注射LPS后接受一次ASPS。LPS攻击6小时后采集血液和肠黏膜样本。测定临床症状、组织学损伤、肠道通透性、TJ超微结构及TJ蛋白表达。

结果

与LPS组小鼠相比,ASPS预处理使临床评分和组织学评分分别提高了390.9%(P<0.05)和57.89%(P<0.05),LPS注射6小时后,内毒素血症小鼠的肠道通透性变化表现为异硫氰酸荧光素-葡聚糖渗漏减少61.93%(P<0.05)。ASPS预处理还可防止LPS诱导的TJ超微结构破坏,相邻细胞间电子致密物质增加,occludin(0.597±0.027比0.103±0.009,P<0.05)和闭合蛋白-1(0.507±0.032比0.125±0.019,P<0.05)持续重新分布和表达,并抑制NF-κB/MLCK途径的激活,表现为NF-κB、磷酸化抑制蛋白κB-α、MLCK和磷酸化肌球蛋白轻链-2的表达分别降低16.06%(P<0.05)、54.31%(P<0.05)、66.10%(P<0.05)和64.82%(P<0.05)。

结论

ASPS预处理可能与抑制NF-κB/MLCK途径及改善内毒素血症中LPS诱导的肠道上皮TJ功能障碍有关。

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