Acute Exposure Of Ozone Induced Pulmonary Injury And The Protective Role Of Vitamin E

Nowadays,with the increase in car ownership and industrial emissions.Ozone(O3)in the lower atmosphere become a major air pollutant in China and has been shown to adversely affect the health of humans and animals,especially for respiratory system.Ozone is derived from important sources of human activity,such as operating motor vehicles,and the fuel and petrochemical industries.Walking in the busy streets,we often see the air slightly light brown and there is a spicy stimulating smell,which is commonly referred to as photochemical smog.Ozone is a major component of photochemical smog generated via a series of complicated photochemical reactions involving nitrogen oxides and sunlight.As a strong oxidant,ozone reacts with almost any biological tissue.When ozone is inhaled,it causes airway inflammation,results in constriction of the airways,increases bronchial reactivity and decreases lung functioning which pose a significant threat to respiratory health.Therefore,this study explores the mechanism of ozone-induced lung inflammation through the use of oxidative damage blocker VE by setting different degrees of ozone exposure to explore the toxic effect concentration of ozone and provides an important experimental basis for the future prevention and treatment to ozone exposure.This study focused on the possibility molecular mechanisms of vitamin E to reduce the level of lung injury in mice,whether it can promote the dissociation of Keapl and Nrf2 in the cytoplasm,and then making Nrf2 into the nucleus to start transcriptiona of antioxidant genes,such as NQO-1,HO-1 and so on to decrease the level of lung injury.In this study,mice were exposed to clean air and three different concentrations of ozone.Oxidative stress(glutathione and malondialdehyde)and Th cytokines in the lung,serum IgE,as well as histopathological examination and the airway hyper-responsiveness(AHR)test were used to reflect inflammation and damage to the lungs of ozone-exposed mice.We then chose an effective concentration of ozone and combined treatment with vitamin E(VE)to explore the underlying mechanism of ozone-induced lung damage.Compared with control group,the results showed that the elevated oxidative stress in lungs was observed in the medium and high concentration ozone exposure groups(0.5 ppm,1.0 ppm),including the increased MDA contents and decreased GSH contents.And the level of IgE in serum,and inflammatory cytokines:IL-4,IL-5 IL-13 and TSLP were also increased.The level of Thl type cytokine:IFN-? was reduced.Which indicated the inmmune balance of Th1/Th2was broken and moved to the Th2 direction.Meanwhile,the number of lymphocytes,eosinophils and neutrophils in BALF increased.H&E staining showed that airway remodeling,collagen deposition,mucus secretion aggravated;pulmonary function test in mice showed the inspiratory,expiratory resistance were increased,and the lung compliance was decreased.The effect of VE on the expression of Nrf2,NQO-1 and HO-1 in the high concentration ozone exposure group could relieve these pathological changes and reduce the airway hyperresponsiveness.In this study,with greater than 0.05 ppm ozone exposure ould induce oxidative stress-induced lung inflammation in mice.In VE-treated mice oxidative stress and lung inflammation were significantly reduced,and the expression of Nrf2 pathway-related antioxidant genes were up-regulated,indicating that Nrf2 pathway is one of the possible mechanisms of VE to protect ozone-induced mice pulmonary inflammation.VE can be used as a protective agent to attenuate the adverse effects of ozone on the lungs.