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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。
Objective To investigate the mechanism of H2O2-induced pulmonary microvascular endothelial cell injury. Methods The effects of H2O2 on the morphology, monolayer permeability, F actin and β AR of rat pulmonary microvascular endothelial cells (RPMC) were observed. Results H2O2 concentration greater than 1mmol·L-1 effect within 48h cells were observed to fall off and rupture. In 10mmol·L-1H2 O2 for 90min, monolayer permeability of RPMVEC increased, F-actin was significantly depolymerized and β AR significantly down-regulated. FOR, anisodamine and CTX could inhibit these changes. Conclusion H2O2 induced RPMVEC shedding and rupture in a concentration and time-dependent manner. The mechanism of H2O2-induced increase of monolayer permeability of RPMVEC is closely related to F-actin depolymerization. Β AR is involved in the regulation of endothelial permeability. FOR, anisodamine and CTX had some protective effects on the increase of RPMVEC monolayer permeability induced by H2O2.