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Protective effects of SUR2B/Kir6.1 potassium channel opener natakalim against RAVECs injuries induced by hypoxia / 中国应用生理学杂志
Chinese Journal of Applied Physiology ; (6): 241-244, 2012.
Article in Chinese | WPRIM | ID: wpr-329898
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective effects of natakalim against rat aortic vascular endothelial cells (RAVECs) injuries induced by hypoxia and its mechanisms.</p><p><b>METHODS</b>Selecting RAVECs as a cell model injured by hypoxia, these RAVECs were divided into 5 groups i.e. control group, hypoxia group, natakalim low, medium and high group. The cell survival rate was determined by MTT assay, con was measured using Griess Assay, RT-PCR was used to examine t he expression of intercellular adhesion molecule-1 (ICAM-1), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1) mRNA in RAVEC.</p><p><b>RESULTS</b>Natakalim could reverse hypoxia-induced changes in endothelial cell function, including increased endothelial cell survival rate and level of NO concentration, significantly inhibited the hypoxia-induced endothelial ICAM-1, ET-1, VEGF mRNA expression levels increased.</p><p><b>CONCLUSION</b>Natakalim have protective effects on hypoxia-induced changes in endothelial cell function, increasing of permeation, excess expression of cell adhesion molecules.</p>
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Aorta / Pharmacology / Propylamines / RNA, Messenger / Cell Hypoxia / Cells, Cultured / Rats, Wistar / Intercellular Adhesion Molecule-1 / Endothelin-1 / Cell Biology Type of study: Prognostic study Limits: Animals Language: Chinese Journal: Chinese Journal of Applied Physiology Year: 2012 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Aorta / Pharmacology / Propylamines / RNA, Messenger / Cell Hypoxia / Cells, Cultured / Rats, Wistar / Intercellular Adhesion Molecule-1 / Endothelin-1 / Cell Biology Type of study: Prognostic study Limits: Animals Language: Chinese Journal: Chinese Journal of Applied Physiology Year: 2012 Type: Article