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嗜酸乳杆菌 NCFM 的表面层蛋白通过 RAW264.7 细胞中的 MAPK 和 NF-κB 信号通路抑制脂多糖诱导的炎症。

Surface-Layer Protein from Lactobacillus acidophilus NCFM Inhibits Lipopolysaccharide-Induced Inflammation through MAPK and NF-κB Signaling Pathways in RAW264.7 Cells.

机构信息

School of Food Science and Technology , Jiangnan University , 1800 Lihu Avenue , Wuxi , Jiangsu 214122 , China.

Jiangsu Institute of Nuclear Medicine , Key Laboratory of Nuclear Medicine, Ministry of Health , 20 Qian Rong , Wuxi , Jiangsu 214063 , China.

出版信息

J Agric Food Chem. 2018 Jul 25;66(29):7655-7662. doi: 10.1021/acs.jafc.8b02012. Epub 2018 Jul 16.

DOI:10.1021/acs.jafc.8b02012
PMID:29975056
Abstract

The objective of our research was to evaluate the molecular mechanism of the anti-inflammatory effects of surface-layer protein (Slp) derived from Lactobacillus acidophilus NCFM in lipopolysaccharide-induced RAW264.7 cells. Our results presented that Slp, with an apparent size of 46 kDa, attenuated the production of TNF-α, IL-1β, and reactive oxygen species (ROS), by inhibiting the MAPK and NF-κB signaling pathways. In addition, 10 μg mL of Slp significantly inhibited NO and PGE production ( P < 0.001) through downregulating the expression levels of iNOS and COX-2 protein. Furthermore, Slp was found to inhibit NF-κB p65 translocation into the nucleus to activate inflammatory gene transcription. These findings suggest that Slp is a potential immune-modulating bioactive protein derived from probiotics and holds promise for use as an additive in functional foods.

摘要

我们的研究目的是评估嗜酸乳杆菌 NCFM 表面层蛋白(Slp)的抗炎作用的分子机制。在脂多糖诱导的 RAW264.7 细胞中,我们的结果表明,Slp 通过抑制 MAPK 和 NF-κB 信号通路,减轻 TNF-α、IL-1β 和活性氧(ROS)的产生。此外,10μg/mL 的 Slp 通过下调 iNOS 和 COX-2 蛋白的表达水平,显著抑制 NO 和 PGE 的产生(P<0.001)。此外,Slp 被发现抑制 NF-κB p65 向核内易位以激活炎症基因转录。这些发现表明 Slp 是一种潜在的免疫调节益生菌来源的生物活性蛋白,有望作为功能性食品的添加剂。

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