黄芩苷通过颈上神经节P2X3受体对心肌缺血诱导的交感兴奋作用的研究。
Study of baicalin on sympathoexcitation induced by myocardial ischemia via P2X3 receptor in superior cervical ganglia.
作者信息
Zhang Jun, Liu Shuangmei, Xu Baohua, Li Guodong, Li Guilin, Huang An, Wu Bing, Peng Lichao, Song Miaomiao, Xie Qiuyu, Lin Weijian, Xie Wei, Wen Shiyao, Zhang Zhedong, Xu Xiaoling, Liang Shangdong
机构信息
Department of Physiology, Medical School of Nanchang University, Nanchang 330006, PR China.
Department of Laboratory Animal, Medical School of Nanchang University, Nanchang 330006, PR China.
出版信息
Auton Neurosci. 2015 May;189:8-15. doi: 10.1016/j.autneu.2014.12.001. Epub 2014 Dec 16.
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.
心肌缺血后，受损的心肌组织释放大量ATP，激活颈上神经节中的P2X3受体，使颈上神经节节后神经元兴奋。交感神经节后传出神经元的兴奋增加了血压和心率，加重了心肌缺血损伤。黄芩苷具有抗炎和抗氧化特性。我们的研究表明，黄芩苷降低了血清CK-MB、cTn-T、肾上腺素和ATP的增量浓度，降低了心肌梗死后颈上神经节中P2X3 mRNA和蛋白上调的表达水平，进而抑制了心肌损伤引发的交感兴奋活动。这些结果表明，作用于P2X3受体的黄芩苷参与了心肌缺血损伤后交感兴奋的传递。黄芩苷可能通过抑制大鼠颈上神经节中的P2X3受体来降低交感活性，从而保护心肌。
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