过氧化氢诱导肺微血管内皮损伤的实验研究

Experimental research on peroxide hydrogen induced injury of pulmonary microvascular endothelial cells

目的 探讨H2 O2 诱导培养肺微血管内皮细胞损伤的机制。方法 观察H2 O2 对大鼠肺微血管内皮细胞 (RP MVEC)的形态、单层通透性、F 肌动蛋白和 β AR的影响。结果 H2 O2 浓度大于 1mmol·L-1作用 48h内观察到细胞脱落和破裂。 10mmol·L-1H2 O2 90min内可使RPMVEC单层通透性增高、F 肌动蛋白发生明显解聚和 β AR显著下调 ;FOR、山莨菪碱和CTX可抑制上述变化。结论 H2 O2引起的RPMVEC脱落与破裂呈浓度和时间依赖性。H2 O2引起RPMVEC单层通透性增高的机制与F 肌动蛋白解聚密切相关 ;β AR参与内皮通透性调节。FOR、山莨菪碱和CTX对H2 O2 引起RPMVEC单层通透性增高有一定的保护作用。

AIM To investigate the mechanism of peroxide hydrogen(H 2O 2) induced injury on the cultured pulmonary microvascular endothelial cell METHODS The effects of H 2O 2 on morphology, monolayer permeability, F actin distribution and β adrenoceptor(β AR) of rat pulmonary microvascular endothelial cell(RPMVEC) were observed RESULTS H 2O 2 in the concentration larger than 1 mmol·L -1 induced detatchment and rupture of RPMVEC within 48 h 10 mg·L -1 of H 2O 2 induced the increased permeability of RPMVEC monolayer, depolymerization of F actin and down regulation of β AR within 90 min Formoterol(FOR), anisodamine and cholera toxin(CTX) inhibited the effects of H 2O 2 CONCLUSION The detatchment and rupture of RPMVEC induced with H 2O 2 depends on the exposed concentration and time The increased permeability of RPMVEC monolayer induced with H 2O 2 is densely correlated with the depolymerization of F actin β AR participates in regulation of endothelial permeability FOR, anisodamine and CTX exert protective action to H 2O 2 induced RPMVEC injury