中文摘要：

目的：探讨胰高血糖素样肽1（glucagon like peptide 1，GLP-1）对脂多糖（1ipopolysaccharide，LPS）诱导的血管内皮细胞（VEC）炎性反应的影响。方法：以体外培养的人动脉VEC为研究模型，将细胞分为四组（对照组、LPS刺激组、LPS±GLP-1组、GLP-1组），Rhodamin-Phalloidin检测肌动蛋白骨架F-actin分布，用苏木素-伊红（HE）染色观察细胞间连接的形态特征，用示踪剂Rhodamine Bisothiocyanate-Dextran检测VECs单层通透性变化改变，酶联免疫吸附实验检测细胞分泌白介素（IL）-6和IL-8的变化。结果：GLP-1（100nM）可减少LPS（1μg／mL）刺激后细胞肌动蛋白骨架F-actin应力纤维的形成，并抑制LPS刺激后细胞间连接的中断。Rhodamine B isothiocyanate-Dextran细胞通透性检测结果显示：GLP-1可明显降低LPS刺激引起的VEC通透性增加[由（2．57±0．19）×10^-5cm／s降至（2．10±0．18）×10^-5cm／s，P〈0．05]。此外，GLP-1可抑制LPS刺激后VEC中炎性细胞因子IL-6和IL-8的表达[分别由（42130±6522）pg／ml降至（27478±5096）pg／ml和（18376±1561）pg／ml降至（14414±927）pg／ml，均P〈0．05]。结论：GLP-1可对抗LPS刺激引起的VEC炎症反应和细胞通透性增加．改善LPS诱导的内皮细胞炎性损伤。

英文摘要：

Objective： To investigate the effect of glucagon like peptide-1 （GLP-1） on lipopolysaccharide （LPS）-induced inflammatory response in the vascular endothelial cells （VECs）. Methods： In vitro cultured human artery VECs were exposed to four groups （control, LPS, LPS ± GLP-1 and GLP-1）. Distribution of cell skeletal protein filamentous actin （F-actin） was detected by Rhodamin-Phalloidin staining. Hematoxylin-eosin staining was used to observe the morphological features of intercellular connections. Endothelial permeability was detected by measuring the flux of Rhodamine B isothiocyanate-Dextran across the VEC monolayers. Interleukin （IL）-6 and IL-8 secretion from cells was determined by using enzyme immunolinked assay （ELISA）. Results： GLP-1 （100 nM） attenuated the formation of F-action stress fiber induced by LPS （1 μg/mL） and inhibited the dissociation of intercellular connections after LPS exposure. Cell permeability test using Rhodamine B isothiocyanate-Dextran indicated that GLP-1 effectively alleviated the hyperpermeability ofVEC monolayer from （2.57 ± 0.19） × 10^-5 cm/s to （2.10 ± 0.18） × 10^-5 cm/s （P 〈 0.05）. In addition, GLP-1 inhibited the secretion of inflammatory cytokines IL-6 and IL-8 induced by LPS [from （42130± 6522） pg/ml to （27478± 5096） pg/ml and （18376 ± 1561） pg/ml to （14414 ± 927） pg/ml, respectively, both P 〈 0.05]. Conclusion： GLP-1 could combat LPS-induced inflammatory responses and the hyperpermeability of VECs, and thereby antagonize LPS-induced pathological cellular injury.