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Protective Role of Glucagon-Like Peptide-1 Against High-Glucose-Induced Endothelial Oxidative Damage

机译:胰高血糖素样肽1对高糖诱导的内皮细胞氧化损伤的保护作用。

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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.
机译:研究胰高血糖素样肽-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(HUVEC)分为对照组(5.5 mmol / L)和高葡萄糖组(19、33或47 mmol / L),分别用不同浓度的葡萄糖培养48小时。用MTT测定法测量细胞活力。通过流式细胞术监测细胞内活性氧(ROS)的水平,并通过用膜联蛋白V-FITC和碘化丙锭染色来测量凋亡细胞的死亡。用蛋白上的细胞间粘附分子1(ICAM-1),VCAM-1和JNK检测培养的细胞。与对照组相比,在33 mM和47 mM下培养时,细胞活力分别降低了20%和37%,而在不同的GLP-1处理组(0.01 L,0.1、1和10 nmol / L)中,细胞活力却增加了)。 GLP-1治疗可显着降低高糖治疗组的ROS水平,但不影响对照组。同时,高糖治疗组细胞凋亡水平升高。在GLP-1处理组中,早期凋亡明显逆转(0.1、1和10 nmol / L)。在10 nmol / L的GLP-1浓度下,晚期细胞凋亡被独特地降低。此外,通过高糖处理,GLP-1还可以降低内皮细胞中ICAM-1,VCAM-1和磷酸JNK的蛋白水平。 GLP-1可以抑制高糖处理诱导的细胞凋亡,减少ROS的产生和JNK-Bax信号通路的激活。

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