| BackgroundRecently,the haze pollution caused by the concentration over-standard of PM2.5 presents a growing trend.The PM2.5 with high concentration is the main reason of haze formation in most of our cities in our country.Due to unreasonable industry and energy structure,it predicates that most of urban residents will live in the heavy polluted environment.Moreover,epidemiological and toxicological studies also indicate that the exposure of PM2.5 has a close relationship with the morbidity and mortality of respiratory diseases.In this situation,it is very important to study the effects on health caused by PM2.5 and the generative mechanism.To study the important impact on oxidative damage and inflammatory response in the lung toxicity process caused by PM2.5,this paper adopts fish oil and vitamin E with the antioxidant and anti-inflammatory effects as an intervention to explore the effects on two interventions in lung toxicity process caused by PM2.5.ObjectiveOur goals are evaluating the intervention effects of fish oil and vitamin E on lung toxicity caused by PM2.5 with this method—using inflammatory reaction,oxidation stress,lung injury and pathological changes of lung tissue caused by the PM2.5 exposure as evaluation indexes.MethodsAcetate membranes are used to collect PM2.5 samples of Xinxiang city from November 2015 to March 2016,and the dried samples are diluted by 0.9% sterilized physiological saline.Sixty-four Wistar male rats were randomly divided into 8 groups: saline control group,PM2.5 exposure group(10.0mg/kg),solvent(corn oil)control group,solvent+PM2.5 group,fish oil(150.0mg/kg)control group,fish oil+PM2.5 group,vitamin E control group(75.0mg/kg)and vitamin E+PM2.5 group.Firstly the rats are given by gavage once a day for 3 weeks with solvent,fish oil or vitamin E.Then rats of control group and rats of PM2.5 group are respectively treated with saline and PM2.5 suspension.The frequency of intratracheal injection is once two day for three times.Finally,after 24 hours in the last instillation,the rats are anaesthetized with chloral hydrate.Moreover,the right lung without irrigation can be made into the pathological section after fixed by 4%formaldehyde solution.Test inflammatory response indexes in the bronchoalveolar lavage fluid(BALF)which contain white blood cell number and intedeukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α);Oxidative stress indexes: superoxide disproportional enzymes(SOD)and 8-epi-prostaglandin F2α(8-epi-PGF2α);Lung injury indexes: the total protein(TP)and lactate dehydrogenase(LDH);.Results(1)Body weights: the rats weights in four control groups are increasing continually during the whole experimental process.However,compared with respective control groups,the trend of the weights growth is becoming smaller in the group of intratracheal injection.(2)White blood cell number: The total number of white blood cells in PM2.5 exposure group are higher than saline control group(P<0.001).The total number of white blood cells in fish oil + PM2.5 group is much lower than that of PM2.5 exposure group and solvent + PM2.5 group(P=0.006,P=0.042).(3)Levels of inflammatory mediators: The levels of IL-1β and TNF-α were significantly higher in the PM2.5 exposure group than in the saline group(P<0.001).The levels of IL-1β and TNF-α in fish oil +PM2.5 group were significantly lower than those in PM2.5 group and solvent +PM2.5 exposure group(all P<0.001).The levels of IL-1β in vitamin E+PM2.5 group were significantly lower than those in PM2.5 group and +PM2.5 group(all P<0.001).(4)Biomarkers of oxidative stress: The activity of SOD in PM2.5 exposure group was significantly lower than that in saline control group(P<0.001).The activity of SOD in fish oil +PM2.5 group was significantly higher than that in PM2.5 exposure group(P=0.041).The levels of 8-epi-PGF2α were significantly higher in the PM2.5 exposure group than in the saline group(P<0.001).(5)Lung injury: There was no significant difference in the levels of TP and LDH in the four control groups.The levels of TP and LDH in PM2.5 exposure group were significantly higher than those in saline control group(all P<0.001).The activity of LDH in solvent +PM2.5 group was significantly lower than that in PM2.5 exposure group(P=0.01).The levels of TP and LDH in fish oil +PM2.5 group were significantly lower than those in PM2.5 exposure group and solven+PM2.5 group(all P<0.001).(6)Histopathological alterations: The alveolar structure is normal and no obvious inflammatory cells exist in four control groups.Besides,the results also indicts that in the lungs of rats in PM2.5 exposure group,the inflammatory cell infiltration,thickened alveolar walls and increased alveolar spaces are found.The pathological sections of fish oil +PM2.5 group showed that some of the alveolar walls were thickened and a small amount of inflammatory cells infiltrated in the lung tissue.Conclusions(1)PM2.5 exposure causes lung toxic effect in rats,represented as increased white blood cell number and levels of IL-1β and TNF-α,decreased levels of SOD and elevated levels of 8-epi-PGF2α,increased levels of TP and LDH in BALF.In addition,PM2.5 exposure can result in infiltration of inflammatory cells into alveoli,destruction of alveolar structure,and thickening of lung interstitium.(2)Pre-treatment with fish oil can ameliorate the toxic effect of PM2.5 as described previously.The toxic effects induced by PM2.5 exposure(except 8-epi-PGF2α).In contrast,Vitamin E only shows inhibitory effect on PM2.5-induced increase in IL-1β. |