Abstract:
Objective:The aim of this study was to investigate the protective effects of licorice flavonoids on cell damage of pulmonary macrophage cells(NR8383)induced by atmospheric fine particulate matter(PM2.5,SRM 2786). Methods:Experimental groups were divided into control group,model group(125 μg/mL SRM 2786),and different concentrations of licorice flavonoids group(3.125,6.25,12.5,25 μg/mL+125 μg/mL SRM 2786)groups,and then cell survival rates were measured by MTT method,observation of cell morphology were examined by optical microscope,Elisa kits were applied to examine cytokine release(TNF-
α,IL-6,IL-1
β)from the NR8383 cells supernatant,nitrate reductase activity(NO),reactive oxygen species(ROS),superoxide dismutase(SOD)and glutathione peroxidase(GSH-PX)were also examined in different NR8383 groups after 24 h treatment. Results:125 μg/mL SRM 2786 significantly decreased cell adherent growth,significantly decreased the cell survival rate,SOD activity and GSH-PX contents compared with the control group,and caused significant increase in the release of TNF-
α,IL-6,IL-1
β,NO and ROS production(
p<0.01). However,3.125~25 μg/mL licorice flavonoids increased cell adhesion with regular shape,and significantly increased the NR8383 cell survival rates,significantly inhibited SRM2786 induced the release of TNF-
α,IL-6,IL-1
β and ROS production,as well as significantly increased SOD activities and GSH-PX contents(
p<0.01),in addition 6.25~25 μg/mL licorice flavonoids significantly reduced the release of NO production induced by SRM 2786 treatment(
p<0.05,
p<0.01). Conclusion:Fine particulate matter PM2.5(125 μg/mL SRM 2786)could significantly inhibit NR8383 cell survival rate,SOD activities and GSH-PX contents,induce the release of inflammatory cytokines as well as promote the production of NO and ROS,however licorice flavonoids(3.125~25 μg/mL)could effectively protect NR8383 cells from these damages induced by PM2.5,the underlying mechanism might correlate with its inhibition of inflammatory response and oxidative stress response.