李莉珊, 马琼锦, 刘洁, 蒋蓉芳, 宋伟民. 维生素E对PM2.5急性染毒致大鼠心血管损伤的保护作用[J]. 上海预防医学, 2017, 29(11): 835-841. DOI: 10.19428/j.cnki.sjpm.2017.11.004
引用本文: 李莉珊, 马琼锦, 刘洁, 蒋蓉芳, 宋伟民. 维生素E对PM2.5急性染毒致大鼠心血管损伤的保护作用[J]. 上海预防医学, 2017, 29(11): 835-841. DOI: 10.19428/j.cnki.sjpm.2017.11.004
Li-shan LI, Qiong-jin MA, Jie LIU, Rong-fang JIANG, Wei-min SONG. Protective effects of Vitamin E on cardiovascular damage in rats caused by ambient PM2.5 acute infections[J]. Shanghai Journal of Preventive Medicine, 2017, 29(11): 835-841. DOI: 10.19428/j.cnki.sjpm.2017.11.004
Citation: Li-shan LI, Qiong-jin MA, Jie LIU, Rong-fang JIANG, Wei-min SONG. Protective effects of Vitamin E on cardiovascular damage in rats caused by ambient PM2.5 acute infections[J]. Shanghai Journal of Preventive Medicine, 2017, 29(11): 835-841. DOI: 10.19428/j.cnki.sjpm.2017.11.004

维生素E对PM2.5急性染毒致大鼠心血管损伤的保护作用

Protective effects of Vitamin E on cardiovascular damage in rats caused by ambient PM2.5 acute infections

  • 摘要:
    目的探讨维生素E(VE)对PM2.5急性染毒致大鼠心血管损伤的干预作用。
    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)、VE对照组、PM2.5染毒组(8.0 mg/kg,以体重计,下同)、PM2.5+VE低、中、高给药组,剂量分别为15.0、30.0、60.0 mg/kg。VE给药组均经VE灌胃28 d后,气管滴注PM2.5悬浊液染毒,隔天1次,共3次。末次染毒24 h后,腹主动脉取血,分析测定血清中白细胞介素1-β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、超敏C反应蛋白(HS-CRP);谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、总超氧化物歧化酶(T-SOD)、血清一氧化氮(NO)、内皮素1(ET-1)和心肌缝隙连接蛋白(Cx43)的含量。
    结果溶剂对照组IL-1β、IL-6、TNF-α、HS-CRP、GSH、GSH-Px、MDA、T-SOD、NO、ET-1及Cx43分别为(68.73±6.21)μg/L、(15.86±0.45)μg/L、(41.12±7.66)μg/L、(1.29±0.26)μg/L、(15.30±2.52)μmol/L、(492.29±28.28)、(10.19±0.74)μmol/L、(272.98±8.59)U/mL,(3.22±0.22)μmol/L、(0.28±0.021)μg/L、(0.42±0.04)μg/L。PM2.5染毒组IL-1β(1 155.98±100.28)μg/L、IL-6(24.94±2.06)μg/L、TNF-α(821.45±14.26)μg/L 、HS-CRP(3.10±0.28)μg/L、MDA(15.88±1.41)μmol/L和ET-1(0.38±0.03)μg/L的释放量升高,GSH(4.62±0.37)μmol/L、GSH-Px(289.28±30.65)、NO(0.97±0.074)μmol/L、Cx43(0.26±0.10)μg/L和T-SOD(239.26±4.97)U/mL含量降低,差异有统计学意义(P < 0.05);与PM2.5染毒组相比,VE给药组的各项指标均有一定缓解作用,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PM2.5染毒可引起大鼠心血管损伤,导致炎性因子、氧化应激指标、血管内皮功能和心肌缝隙链接蛋白的变化,而VE喂饲对PM2.5引起的大鼠急性肺部损伤具有一定的保护作用。

     

    Abstract:
    ObjectiveTo explore the intervention of vitamin E on PM2.5-induced cardiovascular damage in rats.
    MethodsThirty-six SPF male SD rats were randomly divided into six groups including coin oil control group(solvent control group), vitamin E control group, fine particulate matter exposure 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). Each experimental group was exposed to an intra-tracheal instillation for 3 times after 28 days lavage in addition to vitamin E high-dose control group and solvent group. Twenty four hours after the last exposure, the rats were sacrificed and serum was collected, then were measured the ingredients changesBeta 1-beta interleukins (IL-1β), interleukin 6(IL-6), tumor necrosis factor alpha (TNF-alpha), high sensitive C-reaction protein(HS-CRP), Glutathione(GSH), Glutathione peroxidase (GSH-Px), Malondialdehyde(MDA), Superoxide dismutase(T-SOD), NO, Endothelin-1(ET-1) and Connexin 43(Cx43).
    ResultsCompared with solvent group(68.73±6.21)μg/L, (15.86±0.45)μg/L, (41.12±7.66)μg/L, (1.29±0.26)μg/L, (15.30±2.52)μmol/L, (492.29±28.28), (10.19±0.74)μmol/L, (272.98±8.59)U/mL, (3.22±0.22)μmol/L, (0.28±0.021) μg/L and (0.42±0.04)μg/L respectively, the content of IL-1β(1 155.98±100.28 μg/L), IL-6(24.94±2.06 μg/L), TNF-α(821.45±14.26 μg/L), HS-CRP(3.10±0.28 μg/L), MDA(15.88±1.41 μmol/L)and ET-1(0.38±0.03 μg/L)increased and the content of GSH(4.62±0.37 μmol/L), GSH-Px(289.28±30.65)、NO(0.97±0.074 μmol/L), Cx43(0.26±0.10 μg/L) and T-SOD(239.26±4.97 U/mL)decreased in PM2.5 infected-group and the difference was significant between PM2.5 infected-group and solvent group(P < 0.05). Compared with PM2.5 infected control group, the difference of various index of VE groups had statistical significance (P < 0.05), and there was a certain dose-response relationship.
    ConclusionsPM2.5 tracheal drip infections can cause inflammatory damage and oxidative stress changes in rats. VE feeding has protective effects on acute lung damage caused by PM2.5.

     

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