The Effect And Mechanism Of Ginseng Polysaccharide On The Inflammatory Factors Secretion From Mouse Peritoneal Macrophages By Lipopolysaccharide

ObjectiveTo study the anti-inflammatory effects and the mechanism of Ginseng polysaccharide on inflammation factors produced by lipopolysaccharide-induced macrophage in mice.MethodsRAW264.7 cells were inoculated in 6-well plates with the density of 2×10⁴ml^-1.The experiment was divided into blank group,model group,LPS Plus dexamethasone,LPS plus Ginseng polysaccharide group（31.25、62.6、125、250、500μg/ml）.RAW264.7 cells were polarized to inflammatory macrophage by treating with 1μg/mlLPS for 24h.Thecontent of nitricoxide（NO）was assayed by Griess reagent.Enzyme linked immunosorbent assay（ELISA）wereused to assay the content of inflammatory mediators,such as tumor necrosis factor-α（TNF-α）and interleukin-6（IL-6）in cell supernatant.The expressions of iNOS,interleukin-6（IL-6）,tumor necrosis factor-α（TNF-α）mRNA were detected by real-time quantitative PCR（RT-PCR）.And the expressions of p65mitogen-activated protein kinase（p65）protein were determined by using Western blotting.ResultCompared to blank group,the percentages of NO,IL-6,TNF-αof model group were significantly higher（P<0.01）.It means the inflammation model was successfully established.Compared with model group,31.25⁵00μg/ml^-1 of Ginseng polysaccharide in LPS-induced RAW 264.7 cells greatly inhibited the release of inflammatory mediators,such as NO,TNF-αand IL-6（P<0.05,P<0.01）.Compared with the model group,31.25⁵00μg/ml^-1 of Ginseng polysaccharide reduced the concernation of iNOS,interleukin-6（IL-6）,tumor necrosis factor-α（TNF-α）mRNA,（P<0.05,P<0.01）.And the p65 protein were decreased（P<0.01,P<0.05）.ConclusionGinseng polysaccharide can significantly inhibit the over expression of macrophage inflammatory factors NO,TNF-alpha and IL-6,Its mechanism may be related to the inhibition of the expression of related inflammatory factors mRNA and the inhibition of the NF-κB signaling pathway.