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重组可溶性人 CD40L 诱导人脐静脉内皮细胞损伤 被引量:3

Injury effect of recombinant soluble human CD40 ligand on human umbilical vein endothelial cells
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摘要 目的:探讨重组可溶性人CD40L( rshCD40L)对人脐静脉内皮细胞( HUVECs)的损伤作用及其在动脉粥样硬化中的作用。方法:应用rshCD40L刺激人脐静脉内皮细胞12 h;MTS法观察HUVECs的生存活性, ELISA法测内皮细胞E-选择素( E-selectin)、细胞间黏附分子( ICAM)-1、组织因子( TF)、组织因子途径抑制物( TF-PI)表达的变化,比色法测脂质过氧化物丙二醛( MDA)含量及超氧化物歧化酶( SOD)活力。结果:与正常组比较,不同浓度的rshCD40L(0.5、1、2、3 mg/L)对内皮细胞的生存活性无明显影响;0.5 mg/L rshCD40L即可增加内皮细胞E-selectin、sICAM-1、TF、TFPI的分泌,差异有统计学意义( P<0.01),同时增加内皮细胞MDA的含量、降低SOD活性(P<0.05)。结论:0.5~3 mg/L rshCD40L对内皮细胞生存活性无明显影响,但已经引起内皮细胞功能障碍,增加内皮细胞炎症和外源性凝血反应,诱导内皮细胞脂质过氧化物损,使其抗氧化能力下降。 AIM:To investigate the damage in human umbilical vein endothelial cells ( HUVECs) induced by recombinant soluble human CD40 ligand (rshCD40L).METHODS:The cultured HUVECs were treated with rshCD40L for 12 h.The survival activity of the HUVECs was observed by MTS assay.The expression of E-selectin, intercellular ad-hesion molecule (ICAM)-1, tissue factor (TF) and tissue factor pathway inhibitor (TFPI) was measured by ELISA.The activity of superoxide dismutase ( SOD) and the level of malondialdehyde ( MDA) were detected by the methods of thibabi-turic acid (TBA) .RESULTS:Compared with normal group, different concentrations of rshCD40L (0.5, 1, 2, 3 mg/L) had no obvious effect on the survival activity of the HUVECs (P〉0.05).rshCD40L at concentration of 0.5 mg/L promo-ted the secretion of E-selectin, sICAM-1, TF and TFPI in the HUVECs (P〈0.01).rshCD40L at concentration of 0.5 mg/L also increased MDA content and reduced the activity of SOD in the HUVECs (P〈0.05).CONCLUSION:0.5~3mg/L rshCD40L has no obvious effect on endothelial cell survival, but already causes endothelial dysfunction by increas-ing endothelial inflammation and exogenous coagulation reaction, inducing lipid peroxides injury and reducing antioxidant capacity.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2015年第6期1111-1114,共4页 Chinese Journal of Pathophysiology
基金 国家重点基础研究发展计划(973计划)项目(No.2012CB518606)
关键词 人脐静脉内皮细胞 动脉粥样硬化 Recombinant soluble human CD40 ligand Human umbilical vein endothelial cells Atherosclerosis
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