首页> 外文期刊>生物医学研究杂志(英文版) >神经肽Urocortin抑制ECV304细胞和鼠平滑肌细胞的增值
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神经肽Urocortin抑制ECV304细胞和鼠平滑肌细胞的增值

机译:神经肽Urocortin抑制ECV304细胞和鼠平滑肌细胞的增值

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目的:本实验目的在于研究Urocortin(Ucn)对内皮细胞(一种取自人脐静脉内皮细胞HUVEC ECV304)以及大鼠动脉平滑肌细胞(Vascular smooth muscle cells,VSMC)增值的影响,从而探讨其在血管重构(Vascular Remodeling,YR)中的作用.方法:通过四唑盐比色法研究Ucn对内皮细胞以及鼠平滑肌细胞增值的影响.结果:Ucn(10 -7mol/L)抑制ECV304和VSMC细胞的增值.这种抑制作用不依赖于作用时间也不受ATP敏感的钾离子通道阻滞剂glybenclaimide(Gly,10 μmol/L)的影响.结论:提示Ucn不依赖钾离子通道的作用来控制血管重构.可能对高血压的脑或其他器官的并发症有防治作用,可以作为一种新的血管活性药物.%Objective:This study aims to investigate the effects of urocortin (Ucn) on the viability of endothelial cells (ECV304) and rat vascular muscle cells (VSMC). Methods: Rat aortic VSMC were isolated from the rats' thoracic aorta. We studied the effect of Ucn on the viability of ECV304 ceils and VSMC by using a tetrazolium (MTT) assay. Results: Ucn (10-7 mol/L) inhibited the viability of ECV304 cells and VSMC. Inhibition rates are 13% and 15%, respectively( P< 0.05, compared with Control). This inhibition was not dependent on the affecting time and was not affected by the addition of ATP-sensitive potassium channel (KATP channel) blocker, glybenclamide (Gly, 10 mol/L). Conclusion: Ucn inhibits the viability of ECV304 and VSMC.Our results suggest that Ucn may be a new vasoactive agent and may have a beneficial effect in the process of vascular remodeling(VR).
机译:目的:本实验目的在于研究Urocortin(Ucn)对内皮细胞(一种取自人脐静脉内皮细胞HUVEC ECV304)以及大鼠动脉平滑肌细胞(Vascular smooth muscle cells,VSMC)增值的影响,从而探讨其在血管重构(Vascular Remodeling,YR)中的作用.方法:通过四唑盐比色法研究Ucn对内皮细胞以及鼠平滑肌细胞增值的影响.结果:Ucn(10 -7mol/L)抑制ECV304和VSMC细胞的增值.这种抑制作用不依赖于作用时间也不受ATP敏感的钾离子通道阻滞剂glybenclaimide(Gly,10 μmol/L)的影响.结论:提示Ucn不依赖钾离子通道的作用来控制血管重构.可能对高血压的脑或其他器官的并发症有防治作用,可以作为一种新的血管活性药物.%Objective:This study aims to investigate the effects of urocortin (Ucn) on the viability of endothelial cells (ECV304) and rat vascular muscle cells (VSMC). Methods: Rat aortic VSMC were isolated from the rats' thoracic aorta. We studied the effect of Ucn on the viability of ECV304 ceils and VSMC by using a tetrazolium (MTT) assay. Results: Ucn (10-7 mol/L) inhibited the viability of ECV304 cells and VSMC. Inhibition rates are 13% and 15%, respectively( P< 0.05, compared with Control). This inhibition was not dependent on the affecting time and was not affected by the addition of ATP-sensitive potassium channel (KATP channel) blocker, glybenclamide (Gly, 10 mol/L). Conclusion: Ucn inhibits the viability of ECV304 and VSMC.Our results suggest that Ucn may be a new vasoactive agent and may have a beneficial effect in the process of vascular remodeling(VR).

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