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The effects of intermittent hypobaric hypoxia on myocardial ischemia/reperfusion injury and ZFP580 expression / 中国应用生理学杂志
Chinese Journal of Applied Physiology ; (6): 396-400, 2014.
Artigo em Chinês | WPRIM | ID: wpr-243453
ABSTRACT
<p><b>OBJECTIVE</b>To elucidate whether ZFP580 is involved in the cardioprotective effects of intermittent hypobaric hypoxia (IHH) against myocardial ischemia/reperfusion (I/R) injury.</p><p><b>METHODS</b>Thirty two male Wistar rats were randomly divided into 2 groups (n = 16) normoxia control group and IHH preconditioning group. Rats in IHH group were exposed in a hypobaric chamber (equivalent to an altitude of 5 000 m) for a 6 h period each day for 42 d. Plasma was collected and lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) were measured after 2 h of myocardial I/R injury. ZFP580 protein expression in myocardial tissue was assayed by Western blot. Other 8 rats in each group were used to evaluate I/R-induced cardiac infarction by TTC staining. Lentivirus-mediated gene transfection was performed in H9c2 cells 72 h prior to simulated ischemia/reperfusion (SI/R) exposure. The degree of cell apoptosis was determined by annexin V/7-AAD staining and flow cytometry analysis.</p><p><b>RESULTS</b>Compared with normoxia control group, adaptation to IHH attenuated infarct size and plasma leakage of LDH and CK-MB. In addition, ZFP580 expression in the myocardium was up-regulated by IHH. The results of gene transfection showed that ZFP580 overexpression significantly inhibited cells apoptosis induced by SI/R.</p><p><b>CONCLUSION</b>Our findings demonstrate that the cardioprotective effect of IHH against I/R injury is mediated via ZFP580, a novel transcription factor, with anti-apoptotic roles in myocardial cells.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fatores de Transcrição / Traumatismo por Reperfusão Miocárdica / Linhagem Celular / Ratos Wistar / Apoptose / Biologia Celular / Miócitos Cardíacos / Creatina Quinase Forma MB / L-Lactato Desidrogenase / Hipóxia Limite: Animais Idioma: Chinês Revista: Chinese Journal of Applied Physiology Ano de publicação: 2014 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fatores de Transcrição / Traumatismo por Reperfusão Miocárdica / Linhagem Celular / Ratos Wistar / Apoptose / Biologia Celular / Miócitos Cardíacos / Creatina Quinase Forma MB / L-Lactato Desidrogenase / Hipóxia Limite: Animais Idioma: Chinês Revista: Chinese Journal of Applied Physiology Ano de publicação: 2014 Tipo de documento: Artigo