Abstract：
UNASSIGNED: The precise association between lncRNA H19 and ferroptosis in the context of atherosclerosis remains uncertain.
UNASSIGNED: This study is to clarify the underlying process and propose novel approaches for the advancement of therapeutic interventions targeting atherosclerosis.
UNASSIGNED: Assessment of ferroptosis, which entails the evaluation of cell viability using CCK-8 and the quantification of intracellular MDA, GSH, and ferrous ions. Simultaneously, the protein expression levels of assessed by western blot analysis, while the expression level of lncRNA H19 was also determined. Furthermore, HAECs that were cultured with ox-LDL were subjected to Fer-1 interference. HAECs were exposed to ox-LDL and then transfected with H19 shRNA and H19 overexpression vector pcDNA3.1. The level of ferroptosis in the cells was then measured. Then, HAECs were subjected to incubation with ox-LDL, followed by transfection with H19 shRNA and treated with Erastin to assess the levels of ferroptosis, cell viability, and inflammatory factor production. and the ability for blood vessel development.
UNASSIGNED: The survival rate of HAECs in the ox-LDL group was much lower. Ox-LDL resulted in an upregulation of ACSL4 expression in HAECs, while the expression of SLC7A11 and GPX4 decreased.
UNASSIGNED: lncRNA H19 enhances ferroptosis and exacerbates arterial endothelial cell damage induced by LDL.
UNASSIGNED: This study is to clarify the underlying process and propose novel approaches for the advancement of therapeutic interventions targeting atherosclerosis.
UNASSIGNED: Assessment of ferroptosis, which entails the evaluation of cell viability using CCK-8 and the quantification of intracellular MDA, GSH, and ferrous ions. Simultaneously, the protein expression levels of assessed by western blot analysis, while the expression level of lncRNA H19 was also determined. Furthermore, HAECs that were cultured with ox-LDL were subjected to Fer-1 interference. HAECs were exposed to ox-LDL and then transfected with H19 shRNA and H19 overexpression vector pcDNA3.1. The level of ferroptosis in the cells was then measured. Then, HAECs were subjected to incubation with ox-LDL, followed by transfection with H19 shRNA and treated with Erastin to assess the levels of ferroptosis, cell viability, and inflammatory factor production. and the ability for blood vessel development.
UNASSIGNED: The survival rate of HAECs in the ox-LDL group was much lower. Ox-LDL resulted in an upregulation of ACSL4 expression in HAECs, while the expression of SLC7A11 and GPX4 decreased.
UNASSIGNED: lncRNA H19 enhances ferroptosis and exacerbates arterial endothelial cell damage induced by LDL.
摘要：
■在动脉粥样硬化的背景下，lncRNAH19与铁凋亡之间的精确关联仍不确定。
■这项研究旨在阐明潜在的过程，并提出新的方法来推进针对动脉粥样硬化的治疗干预措施。
■铁沉积的评估，这需要使用CCK-8和细胞内MDA的定量来评估细胞活力，GSH,和亚铁离子。同时,通过蛋白质印迹分析评估的蛋白质表达水平，同时还测定了lncRNAH19的表达水平。此外，用ox-LDL培养的HAEC受到Fer-1干扰。将HAECs暴露于ox-LDL，然后用H19shRNA和H19过表达载体pcDNA3.1转染。然后测量细胞中的铁死亡水平。然后，HAEC与ox-LDL孵育，然后用H19shRNA转染并用Erastin处理以评估铁凋亡水平，细胞活力，和炎症因子的产生。和血管发育的能力。
■ox-LDL组HAECs的存活率要低得多。Ox-LDL导致HAECs中ACSL4表达上调，而SLC7A11和GPX4的表达降低。
■lncRNAH19增强铁凋亡并加剧LDL诱导的动脉内皮细胞损伤。
■这项研究旨在阐明潜在的过程，并提出新的方法来推进针对动脉粥样硬化的治疗干预措施。
■铁沉积的评估，这需要使用CCK-8和细胞内MDA的定量来评估细胞活力，GSH,和亚铁离子。同时,通过蛋白质印迹分析评估的蛋白质表达水平，同时还测定了lncRNAH19的表达水平。此外，用ox-LDL培养的HAEC受到Fer-1干扰。将HAECs暴露于ox-LDL，然后用H19shRNA和H19过表达载体pcDNA3.1转染。然后测量细胞中的铁死亡水平。然后，HAEC与ox-LDL孵育，然后用H19shRNA转染并用Erastin处理以评估铁凋亡水平，细胞活力，和炎症因子的产生。和血管发育的能力。
■ox-LDL组HAECs的存活率要低得多。Ox-LDL导致HAECs中ACSL4表达上调，而SLC7A11和GPX4的表达降低。
■lncRNAH19增强铁凋亡并加剧LDL诱导的动脉内皮细胞损伤。
