维生素E对PM_(2.5)急性染毒引起大鼠肺损伤的影响  

EFFECTS OF VITAMIN E ON LUNG INJURY CAUSED BY PM_(2.5) ACUTE EXPOSURE IN RATS

作　　者：李莉珊 马琼锦 杨凌[2] 裴益玲[2] 蒋蓉芳[2] 宋伟民[2] 

机构地区：[1]上海市闵行区疾病预防控制中心,上海201101 [2]复旦大学公共卫生学院公共卫生安全教育部重点实验室,上海200032

出　　处：《营养学报》2016年第3期256-260,266,共6页Acta Nutrimenta Sinica

基　　金：国家自然科学基金(No.81172617)

摘　　要：目的探索维生素E对PM_(2.5)急性气管滴注染毒引起的肺部损伤的干预作用。方法将36只雄性SD大鼠随机分为玉米油对照组(溶剂对照组)、维生素E(VE)高剂量对照组、PM_(2.5)染毒组(8.0mg/kg·bw)、PM_(2.5)+VE低、中、高给药组(剂量分别为15.0,30.0,60.0 mg/kg)。PM_(2.5)+VE给药组均经VE灌胃28d后,气管滴注染毒PM_(2.5)(同时给予VE灌胃),隔日一次,共3次。末次染毒后24 h,行肺灌洗,收集支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF),之后切除肺部,制作肺病理切片,分析测定肺灌洗液中白细胞介素1-β(interleukin 1-beta,IL-1β)、白细胞介素6(interleukin 6,IL-6)、肿瘤坏死因子α(tumor necrosis factor alpha,TNF-α)、乳酸脱氢酶(lactate dehydrogenase,LDH)、大鼠Clara蛋白(clara cell protein,CC16)、丙二醛(malondialdehyde,MDA)、总超氧化物歧化酶(superoxide dismutase,T-SOD)的含量。结果与溶剂对照组的数据[分别为(9.51±0.94)ng/ml,(37.66±4.03)ng/ml,(141.11±15.04)ng/L,(20.84±1.016)nmol/ml,(150.31±5.19)U/L;(5.58±0.20)ng/ml,(231.87±10.02)U/ml]相比,PM_(2.5)染毒组的IL-1β(30.11±0.47)ng/ml、IL-6(99.69±9.49)ng/ml、TNF-α(320.88±12.45)ng/ml、MDA(22.32±0.58)nmol/ml和LDH(378.87±19.61)U/L的释放量升高,CC16蛋白(4.34±0.12)ng/ml和T-SOD(111.81±10.69)U/ml含量降低,差异有统计学意义(P<0.05);与PM_(2.5)染毒组相比,PM_(2.5)+VE给药组的各项指标值差异均有统计学意义(P<0.05),且存在一定的剂量-反应关系。结论急性PM_(2.5)气管滴注染毒可引起大鼠肺部病理损伤,导致炎性因子和氧化应激的变化,而VE喂饲对PM_(2.5)引起的急性肺部损伤具有一定的保护作用。Objective To explore the effects of vitamin E on acute lung injury caused by PM2.s exposure. Methods Thirty-six SPF male SD rats were randomly divided into six groups： corn oil control group （solvent group）, vitamin E high-dose group, fine particulate matter exposed group （8.0 mg/kg·bw）, VE groups with PM2.5 exposure （the low, middle, high experimental dose were 15.0, 30.0, 60.0 mg/kg.bw）. All rats were exposed to an intra-tracheal instillation for 3 times after 28 d lavage. Twenty four hours after the last exposure, the rats were sacrificed, and bronchoalveolar lavage fluid （BALF） was collected. The lungs were resected and the pathological slices were prepared. Then, the biomarkers were measured （1-beta interleukins （IL-1β）, interleukin 6 （IL-6）, tumor necrosis factor alpha （TNF-c0, lactate dehydrogenase （LDH）, Clara cell protein （CC16）, and malondialdehyde （MDA）, superoxide dismutase （T-SOD））. Results Compared with solvent group （9.514-0,94） ng/ml, （37,66±4.03）ng/ml, （141,11±15.04）ng/L, （20,84±1.016）nmol/ml, （150,31±5.19）U/L; （5.58±0.20）ng/ml, （231.87±10.02）U/ml respectively）, the contents of IL-113（30.11±0.47） ng/ml, IL-6（99.69±9.49） ng/ml, TNF-a （320.88±12.45） ng/ml, MDA （22.32±0.58） nmol/ml and LDH （378.874-19.61） U/L were increased and CC16 （4.34±0.12）ng/ml and T-SOD （111.81±10.69） U/ml decreased in PM2.5 exposured group and the differences were sigmflcant statistically between PM2.5 exposed group and solvent group （P〈0.05） . Among the PM2.5 exposured control group and PM2,5＋VE groups, the difference of various indices had statistical significance （P〈0.05）, and there was a certain dose-response relationship. Conclusion PM2.5 tracheal exposure can cause acute lung pathological injury, inflammatory damage and oxidative stress changes. VE is protective against lung damage caused by PM2.5.

关 键 词：维生素E(VE) 大气细颗粒物 气管滴注 肺泡灌洗液 急性肺损伤 

分 类 号：R563[医药卫生—呼吸系统]