灯盏花素对血小板活化因子致肺微血管内皮细胞损伤的影响

Effects of breviscapine on the injury of rat pulmonary microvascular endothelial cells induced by platelet-activating factor

目的 探讨血小板活化因子 (PAF)诱导肺微血管内皮细胞损伤的机制及灯盏花素的干预作用。方法 观察PAF对体外培养大鼠肺微血管内皮细胞 (RPMVEC)的形态、单层通透性、F 肌动蛋白 (F actin)的影响和灯盏花素干预后的变化 ,F actin用流式细胞仪测定。结果 PAF浓度大于 0 1mg·L-1作用 4 8h内观察到细胞脱落和破裂。 10mg·L-1PAF 12 0min内可使RPMVEC单层通透性增高、F actin解聚 ,灯盏花素可抑制上述变化。结论 ①PAF引起RPMVEC脱落和破裂呈时间和剂量依赖性。②PAF引起内皮单层通透性的增高的机制与F actin解聚密切相关。③灯盏花素可抑制PAF引起RPMVEC单层通透性的增高和F actin下降 ,对PAF引起的RPMVEC损伤有一定保护作用。

Aim To investigate the mechanism of platelet-activating factor(PAF) induced injury on the cultured rat pulmonary microvascular endothelial cells(RPMVEC),and the interfering action of breviscapine. Methods RPMVEC were isolated from Wistar rat and cultured in vitro, the effects of PAF on morphology,monolayer permeability and F-actin of RPMVEC were observed, F-actin expression was evaluated by flow cytometry. Results PAF in the concentration over 0.1 mg·L -1 induced detachment and rupture of RPMVEC within 48 h. 10 mg·L -1 of PAF increased permeability of RPMVEC monolayer and induced depolymerization of F-actin within 120 min.Breviscapine inhibited these effects of PAF. Conclusion ①The detachment and rupture of RPMVEC induced by PAF depends on the exposed concentration and time.②The increased permeability of RPMVEC monolayer induced by PAF is significantly correlated with the depolymerization of F-actin. ③The increased permeability of RPMVEC monolayer and depolymerization of F-actin induced by PAF can be markedly inhibited by breviscapine, which exerts protective action on RPMVEC injury induced by PAF.