首页> 外文期刊>American Journal of Physiology >Moderate alcohol consumption induces sustained cardiac protection by activating PKC-epsilon and Akt.
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Moderate alcohol consumption induces sustained cardiac protection by activating PKC-epsilon and Akt.

机译:适度饮酒会通过激活PKC-ε和Akt来诱导持续的心脏保护。

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摘要

C57BL/6 mice were fed 18% ethanol (vol/vol) in drinking water for 12 wk. Isovolumic hearts were subjected to 20 min of ischemia and 30 min of reperfusion on a Langendorff apparatus. There were no differences in baseline hemodynamic function between hearts from ethanol (EtOH)-fed mice and controls. However, prior alcohol consumption doubled recovery of left ventricular developed pressure (68 +/- 8 vs. 33 +/- 8 mmHg for controls; n 10, P < 0.05) and reduced creatine kinase release by half (0.26 +/- 0.04 vs. 0.51 +/- 0.08 U x min(-1) x g wet wt(-1) for controls; n = 10, P < 0.05). EtOH feeding doubled expression of activated protein kinase C epsilon (PKC)epsilon (n = 6, P < 0.05); whereas PKC inhibition blocked protection during ischemia-reperfusion. EtOH feeding also increased expression of Akt three- to fivefold (n = 6, P < 0.05), whereas PKC inhibition prevented increases in Akt kinase activity. We conclude that signaling pathways involving PKC-epsilon are critical for sustained EtOH-mediated cardioprotection and that Akt may be a downstream effector of resistance to myocardial reperfusion injury.
机译:给C57BL / 6小鼠喂食18%乙醇(体积/体积)的饮用水,持续12周。等体积的心脏在Langendorff仪器上进行20分钟的缺血和30分钟的再灌注。用乙醇(EtOH)喂养的小鼠的心脏与对照组之间的基线血液动力学功能没有差异。然而,先前的饮酒使左心室发育压力的恢复翻了一番(对照组为68 +/- 8 vs. 33 +/- 8 mmHg; n 10,P <0.05),肌酸激酶释放降低了一半(0.26 +/- 0.04 vs对照的0.51 +/- 0.08 U x min(-1)xg湿wt(-1); n = 10,P <0.05)。 EtOH喂养使活化蛋白激酶Cε(PKC)ε的表达翻倍(n = 6,P <0.05);而PKC抑制则阻断了缺血再灌注过程中的保护作用。 EtOH喂养还使Akt的表达增加了三到五倍(n = 6,P <0.05),而PKC抑制阻止了Akt激酶活性的增加。我们得出结论,涉及PKC-ε的信号传导途径对于持续的EtOH介导的心脏保护至关重要,而Akt可能是抗心肌再灌注损伤的下游效应器。

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