ox-LDL对PLGF作用内皮细胞释放NO和内皮细胞黏附分子的影响

Effect of oxidative low density lipoprotein on placental growth factor acting on release of nitric oxide and endothelial cell adhesion molecules from human umbilical vein endothelial cells

  • 摘要: 目的: 探讨氧化型低密度脂蛋白对胎盘生长因子-1作用人脐静脉内皮细胞释放一氧化氮和内皮细胞黏附分子的影响。方法: 在ox-LDL(25μg/mL)条件下,应用不同浓度的PLGF-1(20、40、80ng/mL)孵育ECV-304,对照组为内皮细胞未受损时,相同浓度梯度的PLGF-1孵育ECV-304,3h、6h、12h、24h后应用ELISA法检测内皮细胞黏附分子—可溶性细胞间黏附因子-1、可溶性血管内皮细胞黏附因子-1的表达,硝酸盐还原酶法检测NO的表达。结果: 正常生理条件下,PLGF诱导NO和内皮细胞黏附分子的表达,且呈时间(当t=6h达到最理想的分泌量)、浓度依赖关系。在氧化损伤条件下,PLGF诱导NO的表达下降,而内皮细胞黏附分子的表达则增高,以VCAM-1表达增多更为明显。结论: 氧化损伤是动脉粥样硬化的独立危险因素,而PLGF诱导内皮的活化,上调内皮黏附分子的表达,可进一步促使疾病的恶化。故认为抑制PLGF的生物活性可达到控制炎症反应的作用。

     

    Abstract: Objective: To Study the effect of oxidative low density lipoprotein(ox-LDL)on placental growth factor 1(PLGF 1)acting on release of nitric oxide(NO)and endothelial cell adhesion molecules from human umbilical vein endothelial cells(ECV 304). Methods: ECV-304(2×105)were incubated in a RPMI 1640 medium containing 2% heat-inactivated fetal bovine serum with PLGF-1(20,40,80ng/mL)in the absence or presence of ox-LDL.After the cells were cultured for 3,6,12 and 24h,the medium was collected for further use.Levels of soluble inter-cell adhesion molecule 1(sICAM-1)and soluble vascular cell adhesion molecule-1(sVCAM-1)in the supernatant were measured with an ELISA quality kit and expression of NO was analyzed according to its manufacturer’s instructions. Results: PLGF-1 induced secretion of NO and endothelial cell adhesion molecules in a dose-and time-dependent manner,while ox-LDL decreased the NO level.The expression of VCAM-1 was 5-6 folds higher than that in the control group.However,the expression of ICAM-1 was only 2-3 folds higher than that in the control group. Conclusion: Oxidative injury is an independent risk factor for atherosclerosis.PLGF-1 can induce endothelial activation and up-regulate the expression of endothelial adhesion molecules,thus further deteriorating diseases.Inflammatory reaction can be controlled by inhibiting the PLGF-1 bioactivity.

     

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