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热灭活通过肌球蛋白轻链激酶/肌球蛋白轻链途径激活修复脂多糖诱导的肠道上皮屏障损伤。

Heat-Killed Repairs Lipopolysaccharide-Induced Intestinal Epithelial Barrier Damage via MLCK/MLC Pathway Activation.

机构信息

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

Heilongjiang Green Food Science Research Institute, Harbin 150030, China.

出版信息

Nutrients. 2023 Apr 4;15(7):1758. doi: 10.3390/nu15071758.

DOI:10.3390/nu15071758
PMID:37049598
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10097264/
Abstract

Intestinal epithelial barrier function is closely associated with the development of many intestinal diseases. Heat-killed (HK-LP) has been shown to improve intestinal health and enhance immunity. However, the function of HK-LP in the intestinal barrier is still unclear. This study characterized the inflammatory effects of seven HK-LP (1 μg/mL) on the intestinal barrier using lipopolysaccharide (LPS) (100 μg/mL)-induced Caco-2 cells. In this study, HK-LP 6105, 6115, and 6235 were selected, and their effects on the modulation of inflammatory factors and tight junction protein expression (claudin-1, zona occludens-1, and occludin) were compared. The effect of different cultivation times (18 and 48 h) was investigated in response to LPS-induced intestinal epithelial barrier dysfunction. Our results showed that HK-LP 6105, 6115, and 6235 improved LPS-induced intestinal barrier permeability reduction and transepithelial resistance. Furthermore, HK-LP 6105, 6115, and 6235 inhibited the pro-inflammatory factors (TNF-α, IL-1β, IL-6) and increased the expression of the anti-inflammatory factors (IL-4, IL-10, and TGF-β). HK-LP 6105, 6115, and 6235 ameliorated the inflammatory response. It inhibited the nuclear factor kappa B (NF-κB) signaling pathway-mediated myosin light chain (MLC)/MLC kinase signaling pathway by downregulating the Toll-like receptor 4 (TLR4)/NF-κB pathway. Thus, the results suggest that HK-LP 6150, 6115, and 6235 may improve intestinal health by regulating inflammation and TJ proteins. Postbiotics produced by these strains exhibit anti-inflammatory properties that can protect the intestinal barrier.

摘要

肠上皮屏障功能与许多肠道疾病的发展密切相关。已证实热灭活菌(HK-LP)可改善肠道健康并增强免疫力。然而,HK-LP 对肠道屏障的功能仍不清楚。本研究采用脂多糖(LPS)(100μg/ml)诱导 Caco-2 细胞,研究了七种 HK-LP(1μg/ml)对肠道屏障的炎症作用。在本研究中,选择了 HK-LP 6105、6115 和 6235,并比较了它们对调节炎症因子和紧密连接蛋白表达(claudin-1、zonula occludens-1 和 occludin)的影响。还研究了不同培养时间(18 和 48 h)对 LPS 诱导的肠道上皮屏障功能障碍的影响。结果表明,HK-LP 6105、6115 和 6235改善了 LPS 诱导的肠道屏障通透性降低和跨上皮电阻。此外,HK-LP 6105、6115 和 6235 抑制了促炎因子(TNF-α、IL-1β、IL-6),增加了抗炎因子(IL-4、IL-10 和 TGF-β)的表达。HK-LP 6105、6115 和 6235 改善了炎症反应。它通过下调 Toll 样受体 4(TLR4)/NF-κB 通路,抑制核因子 kappa B(NF-κB)信号通路介导的肌球蛋白轻链(MLC)/MLC 激酶信号通路。因此,结果表明 HK-LP 6150、6115 和 6235 可能通过调节炎症和 TJ 蛋白来改善肠道健康。这些菌株产生的后生元具有抗炎特性,可以保护肠道屏障。

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