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目的用大气细颗粒物(PM2.5)刺激人支气管上皮细胞(BEAS-2B细胞),探讨其脂质过氧化作用。方法 PM2.5采自河南省郑州市;实验细胞为人支气管上皮细胞。用0、12.5、25μg/mL的PM2.5刺激BEAS-2B细胞4h后,使用流式细胞仪检测其活性氧(ROS)水平;刺激BEAS-2B细胞8h,用丙二醛试剂盒和超氧化物歧化酶活性测定试剂盒分别检测细胞裂解液中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果 PM2.5作用于BEAS-2B细胞4h,12.5、25μg/mL染毒组ROS水平分别为(6 074.69±41.65)、(7 338.58±168.34),均明显高于对照组的(5 816.66±114.69)(P<0.01);刺激BEAS-2B细胞8h,12.5、25μg/mL染毒组MDA含量分别为(195.44±35.58)、(334.11±26.75)μmol/mg,均明显高于对照组的(71.14±4.21)μmol/mg(P<0.01),同时染毒组SOD活力分别为(100.08±7.54)、(80.03±7.61)U/mg,均低于对照组的(159.91±10.59)U/mg(P<0.01)。结论 PM2.5可以引起BEAS-2B细胞脂质过氧化损伤。
Objective To investigate the effect of lipid peroxidation on human bronchial epithelial cells (BEAS-2B) stimulated by fine particulate matter (PM2.5). Method PM2.5 was collected from Zhengzhou City, Henan Province; experimental cells were human bronchial epithelial cells. BEAS-2B cells were stimulated with 0,12.5,25μg / mL of PM2.5 for 4h, then the level of reactive oxygen species (ROS) was detected by flow cytometry. BEAS-2B cells were stimulated with malondialdehyde (MDA) The activity of the dismutase activity assay kit were detected in the cell lysate malondialdehyde (MDA) content and superoxide dismutase (SOD) activity. Results The ROS levels of PM2.5 cells exposed to BEAS-2B cells for 4 h were significantly higher than those of the control group (12.518 ± 6.66 ± 114.69, (P <0.01). The MDA levels of BEAS-2B cells exposed to 12.5,25μg / mL for 8h were (195.44 ± 35.58) and (334.11 ± 26.75) μmol / mg, (100.08 ± 7.54) and (80.03 ± 7.61) U / mg, respectively, which were all lower than those in the control group (159.91 ± 10.59) U / mg (± 4.21) μmol / P <0.01). Conclusion PM2.5 can cause lipid peroxidation injury in BEAS-2B cells.