中文摘要：

目的：探讨cAMP反应元件结合蛋白（cAMP response element binding protein，CREB）在脂多糖（lipopolysaccharide， LPS）致大鼠肺微血管内皮细胞（rat pulmonary microvascular endothelial cell，RPMVEC）炎症损伤过程中的作用。方法体外分离、培养RPMVEC基础上，Western blot法检测CREB磷酸化CREB水平，伊文思蓝-白蛋白法检测RPMVEC 通透性。结果 LPS刺激RPMVEC后，CREB中Ser133位点磷酸化水平呈时间依赖性地增加，30 min时达到峰值，120 min仍未降至正常水平，加入10μmol＆#183;L-1 V5681（PKA通路特异性抑制剂）共孵育后，CREB 磷酸化几乎被完全抑制， RPMVEC单层通透性明显增加。结论 LPS 能诱导 RPM-VEC中CREB快速磷酸化，PKA 通路介导上述过程，CREB在LPS致RPMVEC炎症损伤过程中可能起到保护作用。

英文摘要：

Aim To investigate the role of cAMP re-sponse element binding protein （CREB）in the injury of rat pulmonary microvascular endothelial cell （RPM-VEC）induced by LPS.Methods RPMVECs were i-solated and cultured in vitro,Western-blot was used to＆amp;nbsp;assay phosphorylation levels of CREB.Endothelial per-meability was determined by measuring the influx of Evans blue-labeled albumin across endothelial mono-layer.Results LPS increased CREB phosphorylation at Ser 1 3 3 in RPMVEC in a time-dependent manner ,＆amp;nbsp;peaked at 30 min,but still higher at 120 min compared with basal control group.Pretreatment of cells with PKA inhibitor V5681 nearly suppressed the CREB phosphorylation stimulated in the presence of LPS,and the monolayer permeability of PMVEC was significantly increased. Conclusions LPS rapidly induces the phosphorylation of CREB in RPMVEC,and PKA me-diates the process.During the process of LPS-stimula-ted injury of RPMVEC,phosphorylation of CREB may play a protective role.