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C-Reactive Protein Can Influence the Proliferation, Apoptosis, and Monocyte Chemotactic Protein-1 Production of Human Umbilical Vein Endothelial Cells

机译:C反应蛋白可以影响人类脐静脉内皮细胞的增殖,凋亡和单核细胞趋化蛋白-1的产生。

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C-reactive protein (CRP) has been shown to be closely associated with coronary heart disease. The serum CRP concentrations of chronic periodontitis (CP) patients were increased due to periodontal inflammation. CRP may be a potential key mediator associating CP with coronary heart disease. This study aimed to investigate the effects of CRP on human endothelial cells in vitro. CRP ranging from 0 to 10 mu g/mL was adopted to imitate the chronic inflammatory conditions of periodontitis. The influences of CRP on proliferation, apoptosis, and monocyte chemotactic protein-1 (MCP-1) production of human umbilical vein endothelial cells (HUVECs) were studied through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and enzyme-linked immunosorbent assay analysis, respectively. Compared to the blank control, 2.5 and 5.0 mu g/mL CRP significantly suppressed cell proliferation by 6.9% and increased apoptosis by 10.2% and 14.6%, respectively (p < 0.05). Concentrations of 7.5 and 10.0 mu g/mL CRP also induced 2.3% HUVEC proliferation suppression (p > 0.05) and significantly increased apoptosis ratio compared to that of the blank control. CRP could promote MCP-1 production of HUVECs in a concentration-dependent manner. The MCP-1 production of 10.0 mu g/mL CRP group was about 15.3% higher than that of the control group. It is concluded that low concentrations of CRP, which appears in CP, inhibits cell proliferation, promotes cell apoptosis, and increases MCP-1 production in endothelium, which may initiate self-repairing function of vascular endothelium following vascular injury process.
机译:C反应蛋白(CRP)已被证明与冠心病密切相关。慢性牙周炎(CP)患者的血清CRP浓度由于牙周炎症而增加。 CRP可能是CP与冠心病相关的潜在关键介体。这项研究旨在研究CRP在体外对人内皮细胞的影响。采用CRP范围从0到10μg / mL来模拟牙周炎的慢性炎症。通过3-(4,5-二甲基噻唑-2-基)-2,5研究了CRP对人脐静脉内皮细胞(HUVEC)增殖,凋亡和单核细胞趋化蛋白-1(MCP-1)产生的影响。 -二苯基溴化四氮唑测定,流式细胞仪和酶联免疫吸附测定分析。与空白对照相比,2.5和5.0μg / mL CRP分别显着抑制了细胞增殖6.9%,并使细胞凋亡分别增加了10.2%和14.6%(p <0.05)。与空白对照相比,浓度为7.5和10.0μg / mL的CRP还可以诱导2.3%的HUVEC增殖抑制(p> 0.05)并显着提高细胞凋亡率。 CRP可以以浓度依赖性方式促进HUVEC的MCP-1产生。 10.0μg / mL CRP组的MCP-1产量比对照组高约15.3%。结论:低浓度的CRP出现在CP中,可抑制细胞增殖,促进细胞凋亡并增加内皮中MCP-1的产生,这可能在血管损伤过程后启动血管内皮的自我修复功能。

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