从植物乳杆菌提取的基因组 DNA 通过抑制 Toll 样受体（ TLR ）介导的丝裂原激活蛋白激酶（ MAPK ）和核因子 - κ B （ NF - κ B ）信号通路减弱牙龈卟啉单胞菌脂多糖（ LPS ）诱导的炎症反应。Genomic DNA Extracted from Lactiplantibacillus plantarum Attenuates Porphyromonas gingivalis Lipopolysaccharide (LPS)-Induced Inflammatory Responses via Suppression of Toll-Like Receptor (TLR)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Nuclear Factor-κB (NF-κB) Signaling Pathways.-医云文献数字医云科研云海量医学决策数据服务

Genomic DNA Extracted from Lactiplantibacillus plantarum Attenuates Porphyromonas gingivalis Lipopolysaccharide (LPS)-Induced Inflammatory Responses via Suppression of Toll-Like Receptor (TLR)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Nuclear Factor-κB (NF-κB) Signaling Pathways.

从植物乳杆菌提取的基因组 DNA 通过抑制 Toll 样受体（ TLR ）介导的丝裂原激活蛋白激酶（ MAPK ）和核因子 - κ B （ NF - κ B ）信号通路减弱牙龈卟啉单胞菌脂多糖（ LPS ）诱导的炎症反应。

Abstract：

In the present study, we aimed to examine the inhibition of genomic DNA from Lactiplantibacillus plantarum (LpDNA) on Porphyromonas gingivalis lipopolysaccharide (PgLPS)-induced inflammatory responses in RAW264.7 cells. Pretreatment with LpDNA for 15 h significantly inhibited PgLPS-induced mRNA expression and protein secretion of interleukin (IL)-1β, IL-6, and monocyte chemoattractant protein-1. LpDNA pretreatment also reduced the mRNA expression of Toll-like receptor (TLR)2 and TLR4. Furthermore, LpDNA inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and the activation of nuclear factor-κB (NF-κB) induced by PgLPS. Taken together, these findings demonstrate that LpDNA attenuates PgLPS-induced inflammatory responses by regulating MAPKs and NF-κB signaling pathways through the suppression of TLR2 and TLR4 expression.

摘要：

在本研究中,我们旨在研究植物乳杆菌基因组DNA(LpDNA)对牙龈卟啉单胞菌脂多糖(PgLPS)诱导的RAW264.7细胞炎症反应的抑制作用.LpDNA预处理15h显著抑制PgLPS诱导的白细胞介素(IL)-1βmRNA表达和蛋白分泌,IL-6和单核细胞趋化蛋白-1。LpDNA预处理还降低了Toll样受体(TLR)2和TLR4的mRNA表达。此外，LpDNA抑制PgLPS诱导的丝裂原活化蛋白激酶（MAPKs）的磷酸化和核因子-κB（NF-κB）的活化。一起来看,这些发现表明，LpDNA通过抑制TLR2和TLR4表达来调节MAPKs和NF-κB信号通路，从而减弱PgLPS诱导的炎症反应。