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β-榄香烯对血管内皮细胞功能紊乱和血管平滑肌细胞异常增殖的影响

β-Elemene improves endothelial cells dysfunction, and abnormal proliferation and migration of vascular smooth muscle cells

  • 摘要: 研究β-榄香烯是否能改善低剪切力(LSS)诱导的血管内皮细胞功能紊乱和氧化型低密度脂蛋白(ox-LDL)诱导的血管平滑肌细胞增殖和迁移。分别采用平行板流动腔和ox-LDL建立血管内皮细胞(ECs)功能紊乱模型和血管平滑肌细胞(VSMCs)增殖和迁移模型,并检测β-榄香烯对ECs功能紊乱和VSMCs增殖迁移的影响。DHE法检测ECs中ROS的活性,DAF-FM DA法检测ECs中NO的活性。Western blot法检测ECs中Akt和ERK的蛋白磷酸化水平。MTT法检测VSMCs的增殖。细胞划痕实验和Transwell实验检测VSMCs的迁移。RT-qPCR法检测VSMCs中MMP-2和MMP-9的基因表达。在ECs中,β-榄香烯可以显著降低LSS诱导的ROS的升高,显著升高LSS诱导的NO的降低,并且降低ERK的磷酸化,并升高Akt的磷酸化。在VSMCs中,β-榄香烯可以显著降低ox-LDL诱导的VSMCs的增殖和迁移,降低MMP-2和MMP-9的基因表达。β-榄香烯可以改善LSS诱导的ECs功能紊乱和ox-LDL诱导的VSMCs增殖和迁移。

     

    Abstract: This study aimed to investigate whether β-elemene could improve the dysfunction of vascular endothelial cells induced by low shear force (LSS), and the proliferation and migration of vascular smooth muscle cells induced by oxidized low-density lipoprotein (ox-LDL). Parallel plate flow chambers and ox-LDL were used to establish vascular endothelial cells (ECs) dysfunction model and vascular smooth muscle cell (VSMCs) proliferation and migration model, respectively, and the effects of β-elemene on ECs dysfunction and VSMCs proliferation and migration were examined. The activity of ROS in ECs was measured by DHE and the activity of NO in ECs was tested by DAF-FM DA. The protein phosphorylation of Akt and ERK in ECs were detected by Western blot. The proliferation of VSMCs was measured by MTT. The migration of VSMCs was examined by cell scratch test and Transwell assay. The gene expression of MMP-2 and MMP-9 in VSMCs was measured by RT-qPCR. In ECs, β-elemene could significantly reduce the LSS-induced increase in ROS, significantly increase the LSS-induced decrease in NO, decrease the phosphorylation of ERK, and increase the phosphorylation of Akt. In VSMCs, β-elemene could significantly reduce the proliferation and migration of VSMCs induced by ox-LDL, and reduce the gene expression of MMP-2 and MMP-9. To conclude, β-elemene can improve the LSS-induced ECs dysfunction and ox-LDL-induced VSMCs proliferation and migration.

     

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