Protective Role of Glucagon-Like Peptide-1 Against High-Glucose-Induced Endothelial Oxidative Damage.
Protective Role of Glucagon-Like Peptide-1 Against High-Glucose-Induced Endothelial Oxidative Damage.
复制标题
胰高血糖素样肽 1 对高血糖诱导的内皮氧化损伤的保护作用。
DOI：
10.1097/md.0000000000002055
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发表时间：
2015-11
期刊：
影响因子：
1.6
通讯作者：
Pan Q
中科院分区：
文献类型：
--
作者：
Guo L;Qiao Y;Zhang L;Pan Q
探讨胰高血糖素样肽-1（GLP-1）对高糖诱导的细胞损伤的保护作用。将人脐静脉内皮细胞（HUVECs）分为对照组（5.5mmol/L）和高糖组（19、33和47 mmol/L），分别加入不同浓度的葡萄糖培养48 h。 MTT法检测细胞活力。通过流式细胞术监测细胞内活性氧（ROS）的水平，并通过用Annexin V-FITC和碘化丙啶染色测量凋亡细胞死亡。用细胞间粘附分子-1（ICAM-1）、血管细胞粘附分子-1（VCAM-1）和JNK蛋白检测培养的细胞。与对照组相比，当在33和47 mM下培养时，细胞活力分别降低20%和37%，而在不同GLP-1处理组（0.01 L、0.1、1和10 nmol/L）中增加。 GLP-1处理显著降低高糖处理组的ROS水平，但对对照组无影响。同时，高糖组细胞凋亡水平升高。GLP-1处理组（0.1、1和10 nmol/L）的早期细胞凋亡显著逆转。 在10 nmol/L的GLP-1浓度下，晚期细胞凋亡唯一减少。 此外，GLP-1还可降低高糖处理的内皮细胞中ICAM-1、VCAM-1和磷酸化JNK的蛋白水平。GLP-1可抑制高糖诱导的细胞凋亡，减少ROS的产生和JNK-Bax信号通路的激活。
To investigate the protective effect of glucagon-like peptide-1 (GLP-1) against cell damage induced by high glucose. Human umbilical vein endothelial cells (HUVECs) were divided into control group (5.5 mmol/L) and high glucose groups (19, 33, or 47 mmol/L), which were cultured with different concentrations of glucose for 48 hours, respectively. Cell viability was measured with MTT assay. Levels of intracellular reactive oxygen species (ROS) were monitored by flow cytometry and apoptotic cell death was measured by staining with Annexin V-FITC and propidium iodide. Cultured cells were detected with intercellular adhesion molecule 1 (ICAM-1), VCAM-1, and JNK on protein. Compared with the control group, cell viability was decreased by 20% and 37%, respectively, when cultured under 33 and 47 mM, while increased in different GLP-1-treated groups (0.01 L, 0.1, 1, and 10 nmol/L). The GLP-1 treatment significantly reduced the ROS level of high glucose treatment group but not impact on the control group. Meanwhile, the level of apoptosis was elevated in the high glucose treatment group. Early apoptosis was significantly reversed in the GLP-1-treated group (0.1, 1, and 10 nmol/L). Late apoptosis was uniquely decreased in the GLP-1 concentrations of 10 nmol/L. Furthermore, GLP-1 could also reduce the protein levels of ICAM-1, VCAM-1, and phospho JNK in the endothelial cells with high glucose treatment. GLP-1 could inhibit cell apoptosis and reduce ROS generation and JNK-Bax signaling pathway activation, which were induced by high glucose treatment.