地塞米松对臭氧化黑碳致肺上皮细胞的氧化损伤和凋亡的保护作用OA北大核心CSTPCD

Objective To study the apoptosis and mechanism of lung epithelial cells induced by exposure to ozone oxidized black carbon(OBC)and explore the therapeutic effect of dexamethasone.Methods A549 cells were divided into seven groups:control group,dexamethasone group and 0,6.5,12.5,25.0,50.0 μg·mL-1OBC treatment groups.All cells were cultured for 24 h.Cell counting kit-8(CCK-8)was used to detect the survival rate of cells.Immunofluorescence was used to detect the activity of reactive oxygen species.Annexin V-FITC/PI two-color fluorescent dye Notation was used to detect apoptotic cells.Real-time quantitative polymerase chain reaction(PCR)was used to detect the expression level of P53,B-cell lymphoma-2(Bcl-2),cysteinyl aspartate specific proteinase-3(caspase-3)mRNA.Western blot was used to detect the expression level of P53,Bcl-2,caspase-3 protein.Results The cell survival rates of 50.0 μg·mL-1 OBC treatment group,control group and dexamethasone group were(12.64±2.45)％,(100.00±0.00)％and(42.39±2.50)％;the reactive oxygen species were(147.00±5.65),(42.82±2.50)and(94.40±4.30)MFI;the apoptosis rates of epithelial cells were(40.50±3.52)％,(5.02±1.15)％and(21.58±2.35)％;the expression of P53 mRNA were 3.81±0.22,1.04±0.02 and 2.03±0.08;the equivalent expression levels of P53 protein were 0.54±0.06,0.14±0.02 and 0.33±0.03.The above indicators in 50.0 μg·mL-1 OBC treatment group showed statistically significant differences compared with control group and dexamethasone group(all P＜0.05).Conclusion OBC exposure leads to oxidative damage of lung epithelial cells and activates their apoptosis related pathways,while dexamethasone has shown good therapeutic effects in vitro experiments.