茶多酚对PM2.5诱导的大鼠肺泡巨噬细胞凋亡的抑制作用

Inhibitory Effect of Tea Polyphenols on Apoptosis of Rat Alveolar Macrophages Induced by PM2.5

关键词:  细颗粒物  茶多酚  肺泡巨噬细胞  氧化损伤  凋亡

Key words:  fine particulate matter  tea polyphenols  alveolar macrophage  oxidative stress  apoptosis

摘要:

目的 研究茶多酚（tea polyphenols，TP）对SRM 2786（PM_2.5标准品）诱导的大鼠肺泡巨噬细胞（NR8383）凋亡的影响及其作用机制。方法 体外培养NR8383细胞，将其分组为对照组、模型组（125 μg·mL^–1的SRM 2786染毒组）及TP干预组（43.75，87.5，175，350 μmol·L^–1 TP+125 μg·mL^–1 SRM 2786），分别干预24 h后，检测细胞存活率、氧化损伤（ROS和NO释放）、炎症因子释放（IL-6、IL-1β及TNF-α）、细胞凋亡率、线粒体损伤及caspase-3/caspase-9活性。结果 与对照组相比，SRM 2786可显著抑制NR8383细胞存活率，促进NO和ROS释放，促进3种炎症因子释放、线粒体损伤、细胞凋亡及caspase-3/caspase-9活性提升。而TP可显著性抑制SRM 2786诱导的NR8383细胞氧化损伤、炎性损伤、线粒体损伤，最终通过抑制caspase-3/caspase-9活性而降低细胞凋亡率，达到提高细胞存活率的目的。结论 TP可通过降低细胞氧化损伤、炎性损伤和caspase-3/caspase-9活性而抑制PM_2.5诱导的NR8383细胞线粒体途径凋亡，提高NR8383细胞活性。

Abstract:

OBJECTIVE To study the effect of tea polyphenols(TP) on apoptosis of rat alveolar macrophages (NR8383) induced by SRM 2786 (PM_2.5 standard) and to explore the underlying mechanism. METHODS The NR8383 cells were cultured in vitro and divided into 6 groups, including control group, model group(125 μg·mL^-1 SRM 2786 exposure group), diverse concentrations of TP groups(43.75, 87.5, 175, 350 μmol·L^-1TP+125 μg·mL^-1 SRM 2786). The following parameters were evaluated after 24 h intervention:cell survival rates, generation of reactive oxygen species(ROS) and NO, production of inflammatory cytokine release(IL-6, IL-1β and TNF-α), apoptosis rate, mitochondrial membrane potential, activities of caspase-3/caspase-9. RESULTS Compared to the control group, SRM 2786 could significantly inhibit the NR8383 cell survival rate, promote the release of NO and ROS, promote the release of three inflammatory factors, mitochondrial damage, apoptosis and increase the activity of caspase-3/caspase-9. In contrast, TP effectively inhibited SRM 2786 induced NR8383 cells oxidative damage, inflammation, mitochondrial damage, and finally elevated cell survival rate via inhibiting caspase-3/caspase-9 activities. CONCLUSION TP can inhibit the mitochondrial apoptosis of NR8383 cells induced by PM_2.5 and improve the activity of NR8383 cells by reducing cell oxidative damage, inflammatory damage and caspase-3/caspase-9 activity.