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首页> 外文期刊>Steroids: An International Journal >BPA disrupts the cardioprotection by 17 beta-oestradiol against ischemia/reperfusion injury in isolated guinea pig hearts
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BPA disrupts the cardioprotection by 17 beta-oestradiol against ischemia/reperfusion injury in isolated guinea pig hearts

机译:BPA扰乱了17β-雌二醇对缺血/再灌注损伤的缺血/再灌注损伤的心脏保护剂

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摘要

Bisphenol A (BPA) is an environmental oestrogen or xenoestrogen (XEs). XEs represent a health risk due to their potential for endocrine disruption and ability to mimic estrogenic activity. The effects of BPA on isolated hearts under normal and ischemia/reperfusion (I/R) conditions were investigated for the first time, with a focus on the effects of BPA and 17 beta-oestradiol (E-2) co-administration on I/R injury. Our results indicated that BPA at 10(-7) M and 10(-5) M did not significantly affect heart rate (HR), coronary flow (CF), lactate dehydrogenase (LDH) or creatine kinase (CK) release in normal or I/R isolated hearts within the 90 min. However, E-2 exerted a protective effect against I/R injury, whereas, BPA inhibited the cardio-protective effects of E-2 on HR, CF, and LDH and CK release. Furthermore, BPA in combination with E-2 aggravated I/R injury by increasing infarct size and causing a more severe ultrastructural disruption as compared to treatment with E-2 alone. Based on our results, we conclude that BPA inhibits the cardio-protective effects of E-2 on I/R-injured hearts, despite not significantly affecting normal or I/R isolated hearts.
机译:双酚A(BPA)是环境雌激素或异雌激素(XES)。由于它们的内分泌破坏和模仿雌激素活性的能力,XES代表了健康风险。 BPA对正常和缺血/再灌注(I / R)条件下的孤立心脏的影响,重点关注BPA和17β-雌二醇(E-2)对I /的影响伤害伤害。我们的结果表明,10(-7)m和10(-5)m的BPA没有显着影响心率(HR),冠状动脉(CF),乳酸脱氢酶(LDH)或肌酸激酶(CK)释放正常或90分钟内的I / R孤立的心。然而,E-2对I / R损伤的保护作用施加了保护作用,而BPA抑制了E-2对HR,CF和LDH和CK释放的心脏保护作用。此外,通过增加梗塞大小并使单独的E-2处理相比,BPA与E / R损伤组合加剧了I / R损伤。根据我们的结果,我们得出结论,BPA抑制了E-2对I / R损伤的心脏的心脏保护作用,尽管没有显着影响正常或I / R孤立的心脏。

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