CAJ | 학술논문

背景:血管内皮细胞衰老、凋亡与再生的平衡对正常血管的功能维持具有极其重要的作用.而线粒体是机体细胞内的重要细胞器,除了合成 ATP 为细胞提供能量外,还控制细胞程序性死亡、以及衰老等多种病理生理的代谢过程. 目的:通过检测脐静脉内皮细胞传代过程中线粒体膜电位与活性氧的改变及其相互关系,从而探讨细胞衰老过程中所产生的功能障碍. 方法:体外培养人脐静脉内皮细胞,选取传代过程中的第2,4,6,8代细胞,采用流式细胞术检测细胞线粒体膜电位及活性氧变化.选取第2,8代细胞行透射电镜检查,观察正常及衰老细胞超微结构的改变. 结果与结论:传代衰老过程中,血管内皮细胞线粒体膜电位逐代降低,而胞内活性氧则出现由增加转而降低的过程.传代后期血管内皮细胞同早期内皮细胞相比,线粒体及内质网明显减少.说明内皮细胞在传代导致的复制性衰老过程中,线粒体膜电位降低,线粒体受损.而在早期传代过程中线粒体轻度受损,而活性氧产生增加,但在线粒体严重受损、功能严重退化过程中,活性氧产生降低.
배경:혈관내피세포쇠로、조망여재생적평형대정상혈관적공능유지구유겁기중요적작용.이선립체시궤체세포내적중요세포기,제료합성 ATP 위세포제공능량외,환공제세포정서성사망、이급쇠로등다충병리생리적대사과정. 목적:통과검측제정맥내피세포전대과정중선립체막전위여활성양적개변급기상호관계,종이탐토세포쇠로과정중소산생적공능장애. 방법:체외배양인제정맥내피세포,선취전대과정중적제2,4,6,8대세포,채용류식세포술검측세포선립체막전위급활성양변화.선취제2,8대세포행투사전경검사,관찰정상급쇠로세포초미결구적개변. 결과여결론:전대쇠로과정중,혈관내피세포선립체막전위축대강저,이포내활성양칙출현유증가전이강저적과정.전대후기혈관내피세포동조기내피세포상비,선립체급내질망명현감소.설명내피세포재전대도치적복제성쇠로과정중,선립체막전위강저,선립체수손.이재조기전대과정중선립체경도수손,이활성양산생증가,단재선립체엄중수손、공능엄중퇴화과정중,활성양산생강저.
@@@@BACKGROUND:Balance among aging, apoptosis and regeneration of vascular endothelial cel s exerts a critical role in maintenance of the function of normal vessels. Mitochondria are a key cel organel e in the body, which cannot only support energy for the cel s via adenosine triphosphate synthesis, but also control the procedure death, aging of cel s as wel as many pathophysical metabolism processes. @@@@OBJECTIVE:To investigate the relationship between mitochondria membrane potentials and reactive oxygen species of endothelial cel s during growing and senescence process in order to explore the dysfunction occurring during the senescence process. @@@@METHODS:Human umbilical vein endothelial cel s were cultured in vitro and passaged. Passages 2, 4, 6 and 8 human umbilical vein endothelial cel s were selected to detect those mitochondria membrane potentials and reactive oxygen species. Levels of reactive oxygen species and mitochondria membrane potentials were checked by flow cytometry. At the same time, passage 2 and 8 cel s were selected for observation of normal and aging ultramicro-morphoses by electron microscope. @@@@RESULTS AND CONCLUSION:During the passage and senescence, mitochondria membrane potentials were decreased gradual y with cel passage, while the levels of reactive oxygen species were increased firstly and then decreased. The number of mitochondria and reticulum was reduced along with cel passage. In replicate aging process, the mitochondrial membrane potential was decreased and the mitochondrion was damaged. At the first time the production of reactive oxygen species was increased, while decreased along with the cel degeneration.