首页> 外文期刊>Autonomic neuroscience: basic & clinical >Study of baicalin on sympathoexcitation induced by myocardial ischemia via P2X3 receptor in superior cervical ganglia
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Study of baicalin on sympathoexcitation induced by myocardial ischemia via P2X3 receptor in superior cervical ganglia

机译:黄ical苷对P2X3受体介导的上颈神经节心肌缺血交感兴奋的研究

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摘要

After the myocardial ischemia, injured myocardial tissues released large quantity of ATP, which activated P2X3 receptor in superior cervical ganglia and made the SCG postganglionic neurons excited. Excitatory of sympathetic postganglionic efferent neurons increased the blood pressure and heart rates, which aggravated the myocardial ischemic injury. Baicalin has anti-inflammatory and anti-oxidant properties. Our study showed that baicalin reduced the incremental concentration of serum CK-MB, cTn-T, epinephrine and ATP, decreased the up-regulated expression levels of P2X3 mRNA and protein in SCG after MI, and then inhibited the sympathetic excitatory activity triggered by MI injury. These results indicated that baicalin acted on P2X3 receptor was involved in the transmission of sympathetic excitation after the myocardial ischemic injury. Baicalin might decrease sympathetic activity via inhibiting P2X3 receptor in rat SCG to protect the myocardium.
机译:心肌缺血后,受损的心肌组织释放大量的ATP,激活上颈神经节中的P2X3受体,并使SCG神经节后神经元兴奋。兴奋性交感神经节后传出神经元增加血压和心率,加重心肌缺血性损伤。黄ical苷具有抗炎和抗氧化特性。我们的研究表明,黄ical苷降低MI后SCG中血清CK-MB,cTn-T,肾上腺素和ATP的增量浓度,降低P2X3 mRNA和蛋白的表达水平,进而抑制MI引起的交感兴奋性活动。受伤。这些结果表明,黄ical苷对P2X3受体的作用参与了心肌缺血损伤后交感神经兴奋的传递。黄ical苷可能通过抑制大鼠SCG中的P2X3受体来降低交感活性,从而保护心肌。

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