Objective: To investigate the protective effects of paeoniflorin against PM2.5-induced damage in BEAS-2B cells and explore the possible mechanism.
Methods: With a factorial design, this study was performed to observe the protective effects of different doses of paeoniflorin against PM2.5-induced BEAS-2B cell growth inhibition and the effects of paeoniflorin on the contents of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS) in the cell cultures.
Results: Exposure to increased PM2.5 concentrations caused significant decrease in the cell survival rate (P<0.05) with a clear dose-response relationship (r=-0.759, P<0.05). Treatment of the cells with paeoniflorin significantly attenuated PM2.5-induced inhibition of BEAS-2B cell survival (P<0.05), but the effect of paeoniflorin was not dose-dependent (P>0.05). PM2.5 exposure also significantly increased the contents of MDA and intracellular ROS (P<0.05), and paeoniflorin obviously antagonized these effects of PM2.5.
Conclusion: Paeoniflorin can protect BEAS-2B cells from PM2.5-induced growth inhibition, and the mechanism might be related to the anti-oxidant effects of paeoniflorin.
目的: 探索芍药苷对PM2.5诱导人支气管上皮细胞(BEAS-2B细胞)损害的保护作用及其机制。
方法: 采用析因设计，分别利用MTT法，TBA法及化学荧光法，测定不同剂量芍药苷对PM2.5染毒所致BEAS-2B细胞生长抑制，细胞培养上清中丙二醛(MDA)及细胞内活性氧(ROS)的含量的影响。
结果: 随着PM2.5干预浓度水平的增高，细胞存活率显著性降低(P < 0.05)，并呈剂量反应关系(r=-0.759，P < 0.05)，随着共处理芍药苷干预浓度的增高，PM2.5诱导BEAS-2B细胞存活率下降的幅度明显降低(P < 0.05)，但未观察到剂量-反应关系(P > 0.05)；同时发现PM2.5染毒可致细胞培养上清中MDA，细胞内ROS含量均显著增高(P < 0.05)，芍药苷高浓度干预时，细胞培养上清中MDA，细胞内ROS含量较染毒对照组均显著性降低(P < 0.05)。
结论: 芍药苷对PM2.5所致BEAS-2B细胞的生长抑制有明显的保护作用，其机制可能与芍药苷抗氧化作用有关。