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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
引用本文: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].现代生物医学进展,2014,14(24):4652-4655.
作者姓名:段岩  刘新宇  李凤华  惠丽超  王硕  张晓妍
作者单位:辽宁医学院附属第一医院内分泌和代谢科
基金项目:辽宁省优秀硕士论文课题(2012071)
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(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,P0.05]。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P0.05]。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。

关 键 词:胰高血糖素样肽-l  血管内皮细胞  炎性反应  脂多糖

Effect of Glucagon Like Peptide-1 on Lipopolysaccharide-induced Inflammatory Response in the Vascular Endothelial Cells
DUAN Yan,LIU Xin-yu,LI Feng-hu,HUI Li-chao,WANG Shuo,ZHANG Xiao-yan.Effect of Glucagon Like Peptide-1 on Lipopolysaccharide-induced Inflammatory Response in the Vascular Endothelial Cells[J].Progress in Modern Biomedicine,2014,14(24):4652-4655.
Authors:DUAN Yan  LIU Xin-yu  LI Feng-hu  HUI Li-chao  WANG Shuo  ZHANG Xiao-yan
Abstract: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.
Keywords:Glucagon like peptide-1(GLP-1)  Vascular endothelial cells(VEC)  Inflammatory response  Lipopolysaccharide
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