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

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Surface-Layer Protein from Lactobacillus acidophilus NCFM Inhibits Lipopolysaccharide-Induced Inflammation through MAPK and NF-κB Signaling Pathways in RAW264.7 Cells
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2018-07-05 00:00:00 , DOI: 10.1021/acs.jafc.8b02012
Huifang Wang ₁ , Li Zhang ₂ , Shichen Xu _{1,

2} , Jie Pan ₁ , Qiuxiang Zhang ₁ , Rongrong Lu ₁

Affiliation

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^–1 of Slp significantly inhibited NO and PGE₂ 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.

中文翻译：

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

我们研究的目的是评估嗜酸乳杆菌NCFM衍生的表面层蛋白（Slp）在脂多糖诱导的RAW264.7细胞中抗炎作用的分子机制。我们的研究结果表明，Slp的表观大小为46 kDa，可通过抑制MAPK和NF-κB信号通路来减弱TNF-α，IL-1β和活性氧（ROS）的产生。此外，10μgmL ^–1的Slp可显着抑制NO和PGE _2的产生（P<0.001）通过下调iNOS和COX-2蛋白的表达水平。此外，发现Slp抑制NF-κBp65易位进入细胞核以激活炎性基因转录。这些发现表明，Slp是一种源自益生菌的潜在的免疫调节生物活性蛋白，并有望在功能性食品中用作添加剂。

更新日期：2018-07-05

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