某鱼油产品对细颗粒物引起的急性肺损伤的影响

Effect of a Fish Oil Product on Acute Lung Injury Caused by Fine Particulate Matters

[目的]探索某鱼油产品对细颗粒物(PM2.5)气管滴注染毒引起的肺部急性毒性的干预作用。[方法]将36只雄性SD大鼠随机分为6组,即溶剂(玉米油)对照组、鱼油(0.60 g/kg)对照组、PM2.5染毒(8.0 mg/kg)对照组、PM2.5+低、中、高剂量(0.15、0.30、0.60 g/kg)鱼油给药组。PM2.5染毒对照组、鱼油给药组分别经正常饲养、鱼油灌胃28 d后,行气管滴注染毒PM2.5,滴注量为8.0 mg/kg,隔天1次,共3次。鱼油对照组行鱼油灌胃35 d,溶剂对照组先后行玉米油灌胃(28 d)和生理盐水气管滴注(7 d)。末次染毒后24 h,行肺灌洗,收集支气管肺泡灌洗液,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1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、Clara细胞蛋白(CC16蛋白)、超敏C反应蛋白(hs-CRP)、丙二醛(MDA)、总超氧化物歧化酶(T-SOD)的含量。[结果]与溶剂对照组相比:PM2.5染毒对照组大鼠炎症指标IL-1β、IL-6、hs-CRP和TNF-α升高,CC16蛋白降低;氧化应激指标T-SOD降低(均P<0.05)。与PM2.5染毒对照组相比:各剂量的鱼油给药组大鼠IL-1β、IL-6、hs-CRP和TNF-α的释放量均降低,CC16蛋白含量升高,T-SOD含量升高(均P<0.05)。各实验组间MDA含量差异无统计学意义(P>0.05)。[结论]PM2.5气管滴注染毒可以引起大鼠肺部急性损伤,导致炎性因子和氧化应激的变化,该种鱼油产品喂饲对PM2.5急性染毒引起的大鼠肺部损伤具有一定的保护作用。

[ Objective ] To examine the intervention effect of a fish oil product on acute lung injury induced by intratracheal instillation of fine particulate matter with median aerodynamic diameter 〈2.5 μm （PM2.5）. [ Methods ] Thirty-six male SD rats were randomly divided into six groups, including solvent （corn oil） control group, fish oil （0.60 g/kg） control group, PM2.5 exposure （$.Omg/kg） group, and PM2.5 plus fish oil groups at low, middle, high doses offish oil （0.15, 0.30, 0.60 g/kg）. The PM2.5 exposure group and the PM2.5 plus fish oil groups were administered with 8.0 mg/kg PM2.5 by intratracheal instillation for three times, once every other day, after 28 days of normal feeding or fish oil lavage. The fish oil control group was administered with fish oil by gavage for 35 d; the solvent control group was administered with corn oil by gavage for 28 d and saline by intratracheal instillation for 7 d. Twenty-four hours after the last exposure, the rats were sacrificed and brochoalveolar lavage fluid （BALF） were collected. Lung biopsy samples were resected to measure interleukin-1 beta （IL-1β）, interleukin-6 （IL-6）, tumor necrosis factor alpha （TNF-a）, Clara cell protein （CC 16）, hypersensitive C-reactive protein （hs-CRP）, malondialdehyde （MDA）, and superoxide dismutase （T-SOD）. [ Results ] Compared with the solvent group, IL-1β, IL-6, hs-CRP, and TNF-α were increased whereas CC16 and T-SOD were decreased in the PM2.5 exposure group （all P 〈 0.05）. Compared with the PM2.5 exposure group, IL-1 β, IL-6, hs-CRP, and TNF-α were lower whereas CC16 and T-SOD were higher in various PM2.5 plus fish oil groups （all P〈 0.05）. No differences in MDA were found among the experiment groups. [ Conclusion ] PM2.5 intratracheal instillation could induce acute lung injury in rats such as inflammatory damage and oxidative stress changes. The selected fish oil product shows protective effects on the lung damage caused by PM2.5.