| Background:Ambient air pollution is a major public health problem worldwide.It is estimated that more than 90%of the world’s population currently live in areas where the concentration of air pollutants exceeds the limits of the WHO.A large number of epidemiological studies have linked airborne particulate matters pollution with respiratory diseases and cardiovascular diseases,such as COPD and asthma.PM2.5 receives widespread attention in recent years,but the complex mechanism of the adverse health effects caused by PM2.5 is not fully understood.In this study,HBE model and HUVEC model were established to explore the toxicological effects and mechanism of airborne particulate matters and indoor PM2.5 from the printers on respiratory diseases and cardiovascular diseases.Method 1:HBE cells model1.Effects of airborne particle matters and indoor PM2.5 from the printers on HBE cells.Collected airborne PM2.5,airborne TSP and indoor PM2.5 from the printers of Nanchang University.Added them into a working solution with a concentration of 100 μg/mL,and the control group(cell hole without sample),TSP group(airborne TSP),PRM group(indoor PM2.5 from the printers)and PM group(airborne PM2.5)were set.2.Effects of different concentration of indoor PM2.5 from the printers on HBE cells.Collected indoor PM2.5 from the printers to make a suspension,and the control group(cell hole without sample),PRL group(low concentration 25 μg/mL),PRM group(medium concentration 100 μg/mL)and PRH group(high concentration 400μg/mL)were set.3.The CCK-8 was used to detect the effects of airborne TSP,indoor PM2.5 from the printers and airborne PM2.5 on the survival rate of HBE cells.The changes of SOD activity and the content of MDA in HBE cells were detected 7 hours after exposure.ELISA was used to detect the protein expression of inflammation related factors IL-1β,IL-6,TNF-α,IL-2 in HBE cells.Western blot was used to detect the inflammatory proteins COX2,p-p65/p65,and Bax/Bcl-2.Method 2:HUVEC cells model1.Effects of airborne particle matters and indoor PM2.5 from the printers on HUVEC cells.Collected airborne PM2.5,airborne TSP and indoor PM2.5 from the printers of Nanchang University.Added them into a working solution with a concentration of 100 μg/mL,and the control group(cell hole without sample),TSP group(airborne TSP),PRM group(indoor PM2.5 from the printers)and PM group(airborne PM2.5)were set.2.Effects of different concentration of indoor PM2.5 from the printers on HUVEC cells.Collected indoor PM2.5 from the printers to make a suspension,and the control group(cell hole without sample),PRL group(low concentration 25 μg/mL),PRM group(medium concentration 100 μg/mL)and PRH group(high concentration 400、μg/mL)were set.3.The CCK-8 was used to detect the effects of airborne TSP,indoor PM2.5 from the printers and airborne PM2.5 on the survival rate of HUVEC cells.The changes of SOD activity and the content of MDA in HUVEC cells were detected 7 hours afterexposure.ELISA was used to detect the protein expression of inflammation related factors IL-1β,IL-6,TNF-α,IL-2 in HUVEC cells.Western blot was used to detect the inflammatory proteins COX2,p-p65/p65,and Bax/Bcl-2.Result 1:HBE cells model1.Through the CCK-8 proliferation experiment,it was found that airborne TSP,indoor PM2.5 from the printers and airborne PM2.5 could inhibit the survival rate of HBE cells.Compared with the control group,the smallest airborne PM2.5 significantly reduced the survive rate of HBE cells.Although the toxicity of indoor PM2.5 from the printers was weaker than airborne PM2.5.With the increase of concentration of indoor PM2.5 from the printers increases,the survival rate of HBE cells gradually decreased.2.The results of oxidative stress experiments showed that the SOD activity decreased and the content of MDA increased when the particle size decreased.Although the ability of indoor PM2.5 from the printers in inducing oxidative stress in HBE cells was weaker than airborne PM2.5,high-concentration indoor PM2.5 from the printers significantly reduced SOD activity and significantly increased the content of MDA in HBE cells.3.ELISA results showed that,compared with the control group,with the decrease in particle size,the secretion of pro-inflammatory factors IL-1β,IL-6,TNF-α gradually increased,and the secretion of anti-inflammatory factor IL-2 gradually decreased in HBE cells.Although the ability of indoor PM2.5 from the printers to induce cell inflammation was weaker than airborne PM2.5,with the concentration of indoor PM2.5 from the printers increased,the secretion of pro-inflammatory factors IL-1β,IL-6,TNF-α gradually increased,and the secretion of the anti-inflammatory factor IL-2 gradually decreased in the HBE cells.4.Western blot results showed that compared with the control group,the smaller the airborne particle matters was,the higher expression of COX2 and p-p65/p65 in the inflammatory pathway and Bax/Bcl-2 protein in the apoptotic pathway were.Although the indoor PM2.5 from the printers on inflammatory effect and the ability to induce cell apoptosis were weaker than the airborne PM2.5,the experiment found that the high concentration indoor PM2.5 from the printers had a strong inflammatory effect and caused apoptosis.Result 2:HUVEC cell model1.Through the CCK-8 proliferation experiment,it was found that airborne TSP,indoor PM2.5 from the printers and airborne PM2.5 could inhibit the survival rate of HUVEC cells.Compared with the control group,the smallest airborne PM2.5 significantly reduced the survive rate of HUVEC cells.Although the toxicity of indoor PM2.5 from the printers was weaker than airborne PM2.5,with the increases of concentration of indoor PM2.5 from the printers,the survival rate of HUVEC cells gradually decreased.2.The results of oxidative stress experiments showed that the SOD activity decreased and the content of MDA increased when the particle size decreased.Although the ability of indoor PM2.5 from the printers in inducing oxidative stress in HUVEC cells was weaker than airborne PM2.5,high-concentration indoor PM2.5 from the printers significantly reduced SOD activity and significantly increased the content of MDA in HUVEC cells.3.ELISA results showed that,compared with the control group,with the decrease in particle size,the secretion of pro-inflammatory factors IL-1β,IL-6,TNF-α gradually increased,and the secretion of anti-inflammatory factor IL-2 gradually decreased in HUVEC cells.Although the ability of indoor PM2.5 from the printers to induce cell inflammation was weaker than airborne PM2.5,with the concentration of indoor PM2.5 from the printers increased,the secretion of pro-inflammatory factors IL-1β,IL-6,TNF-α gradually increased,and the secretion of the anti-inflammatory factor IL-2 gradually decreased in the HUVEC cells.4.Western blot results showed that compared with the control group,the smaller the airborne particle matters was,the higher expression of COX2 and p-p65/p65 in the inflammatory pathway and Bax/Bcl-2 protein in the apoptotic pathway were.Although the indoor PM2.5 from the printers on inflammatory effect and the ability to induce cell apoptosis were weaker than the airborne PM2.5,the experiment found that the high concentration indoor PM2.5 from the printers had a strong inflammatory effect and caused apoptosis.Conclusion:The smaller the particle size is,the stronger the toxicity it has.And it can significantly induce oxidative damage,inflammation and apoptosis of HBE cells and HUVEC cells.In addition,oxidative damage,inflammation,and apoptosis may be important mechanisms for airborne particulate matters and indoor PM2.5 from the printers to cause respiratory diseases and cardiovascular diseases. |
PDF Full Text Request