文章摘要
段岩 刘新宇 李凤华 惠丽超 王硕 张晓妍.胰高血糖素样肽l对脂多糖诱导的血管内皮细胞炎性反应的影响[J].,2014,14(24):4652-4655
胰高血糖素样肽l对脂多糖诱导的血管内皮细胞炎性反应的影响
Effect of Glucagon Like Peptide-1 on Lipopolysaccharide-inducedInflammatory Response in the Vascular Endothelial Cells
  
DOI:
中文关键词: 胰高血糖素样肽-l  血管内皮细胞  炎性反应  脂多糖
英文关键词: Glucagon like peptide-1(GLP-1)  Vascular endothelial cells(VEC)  Inflammatory response  Lipopolysaccharide
基金项目:辽宁省优秀硕士论文课题(2012071)
作者单位
段岩 刘新宇 李凤华 惠丽超 王硕 张晓妍 辽宁医学院附属第一医院内分泌和代谢科 
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中文摘要:
      目的:探讨胰高血糖素样肽l (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 B isothiocyanate-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(100 nM)可减少LPS(1 ug/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)× 10-5 cm/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 1ipopolysaccharide (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 fromcells 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 ug/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 of VEC 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.
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