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首页> 外文期刊>Journal of receptor and signal transduction research >β2-Adrenoceptor confers cardioprotection against hypoxia in isolated ventricular myocytes and the effects depend on estrogenic environment
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β2-Adrenoceptor confers cardioprotection against hypoxia in isolated ventricular myocytes and the effects depend on estrogenic environment

机译:β2-肾上腺素能受体使心肌细胞免受缺氧侵袭,其作用取决于雌激素环境

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摘要

Estrogen plays a cardioprotective role in female rat hearts subjected to ischemia/reperfusion injury. The its effects are, at least partially, associated with decreased cardiomyocyte contraction and increased expression of β_2-adrenoceptor (β_2-AR). We tested whether β_2-AR could be involved in cardioprotection against ischemic damage and whether the roles of β_2-AR were dependent on estrogenic environment. We first determined the effects of hypoxia/reoxygenation (H/R) on cardiomyocyte shortening in female rats. We then determined the roles of β_2-AR in cardiomyocyte shortening, lactate dehydrogenase (LDH) release in culture medium, and cell death during hypoxia in isolated myocytes from female rats. We further determined the effects of estrogen on the roles of β_2-AR during hypoxia. H/R induced short-term hibernation and stunning at the level of ventricular myocytes from normal female rats. Inhibition of β_2-AR with ICI118,551 significantly elevated adrenergic contractile reserve, myocardial injury, and cell death in normal female rats during hypoxia, whereas ovariectomy (OVX) prominently enhanced myocyte contraction, myocardial injury, and cell death, and deprived the alternations in normal female rats. These changes were restored to normal by estrogen replacement (OVXE_2). These data suggest that β_2-AR may be involved in the cardioprotection against ischemic damage, and the cardioprotection may depend on estrogenic environment.
机译:雌激素在遭受缺血/再灌注损伤的雌性大鼠心脏中起心脏保护作用。其作用至少部分与心肌细胞收缩减少和β_2-肾上腺素能受体(β_2-AR)表达增加有关。我们测试了β_2-AR是否可以参与抗缺血性损伤的心脏保护作用,以及β_2-AR的作用是否取决于雌激素环境。我们首先确定了缺氧/复氧(H / R)对雌性大鼠心肌细胞缩短的影响。然后,我们确定了β_2-AR在缩短雌性大鼠心肌细胞中心肌细胞缩短,乳酸脱氢酶(LDH)在培养基中释放以及缺氧期间细胞死亡中的作用。我们进一步确定了雌激素对缺氧期间β_2-AR的作用。 H / R引起正常雌性大鼠心室肌细胞水平的短期冬眠和惊吓。在缺氧状态下,ICI118,551对β_2-AR的抑制作用显着提高了正常雌性大鼠的肾上腺能收缩储备,心肌损伤和细胞死亡,而卵巢切除术(OVX)显着增强了心肌细胞的收缩,心肌损伤和细胞死亡,并且剥夺了交替发生的作用。正常的雌性大鼠。这些变化通过雌激素替代(OVXE_2)恢复到正常状态。这些数据表明β_2-AR可能参与针对缺血性损伤的心脏保护,并且心脏保护可能取决于雌激素环境。

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