Antagonistic Effect of Glycyrrhiza Polysaccharides on LPS-induced Inflammation Damagein A549 Cells
Glycyrrhiza is one of the most widely used herbaceous plants in the world,and its main ex-tract of glycyrrhiza polysaccharide is a polysaccharide compound with various biological activities.Aims to ex-plore the molecular mechanism of the antagonistic effect of glycyrrhiza polysaccharide(GP)on lipopolysaccha-ride(LPS)induced inflammation of A549 cells,and provide a theoretical basis for the treatment of pulmonary in-flammatory diseases.The crude extract of glycyrrhiza polysaccharides was extracted using water extraction and alcohol precipitation method.Using the cell proliferation detection CCK 8 kit to detect the effects of different concentrations of glycyrrhiza polysaccharides and LPS on the viability of A549 cells.The expressions of TNF-αand IL-6 factors in cells was detected by enzyme-linked immunosorbent assay(ELISA).The expression of NF-κB,IL-1β and IL-6 mRNA levels was detected by real time fluorescence quantitative PCR in A549 cells.The results showed that compared with the control group,glycyrrhiza polysaccharide were promoted an increase in A549 cell viability,while LPS treatment significantly reduced A549 cell viability.The ELISA test results showed that compared to the control group,the content of cell inflammatory factors TNF-α and IL-6 signifi-cantly increased by LPS treated.Further,the content of TNF-α and IL-6 were significantly reduced by LPS and glycyrrhiza polysaccharide and complex treatment in A549 cells.In addition,the real-time fluorescence quantita-tive PCR results showed that the expression of IL-6、IL-1β and NF-κB inflammatory factors were significantly increased in the LPS group,and the mRNA expressions of IL-6、IL-1β and NF-κB inflammatory factors were significantly decreased after treatment with glycyrrhiza polysaccharide.Glycyrrhiza polysaccharide could signifi-cantly reduce the expression of inflammatory factor mRNA,compared with the LPS group.In summary,glycyr-rhiza polysaccharide have an antagonistic effect on LPS induced inflammatory damage possibly through inhibit-ing NF-κB signal pathway in A549 cells.
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