Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia

黄芩苷通过背根神经节抑制心肌缺血引起的交感神经兴奋反射

阅读:5
作者:Lifang Zou, Xinyao Han, Shuangmei Liu, Yingxin Gong, Bing Wu, Zhihua Yi, Hui Liu, Shanhong Zhao, Tianyu Jia, Lin Li, Huilong Yuan, Liran Shi, Chunping Zhang, Yun Gao, Guilin Li, Hong Xu, Shangdong Liang

Abstract

Myocardial ischemia (MI) is one of the major causes of death in cardiac diseases. Purinergic signaling is involved in bidirectional neuronal-glial communication in the primary sensory ganglia. The sensory neuritis of cardiac afferent neurons in cervical dorsal root ganglion (cDRG) interacts with cardiac sympathetic efferent postganglionic neurons, forming feedback loops. The P2Y12 receptor is expressed in satellite glial cells (SGCs) of DRG. Baicalin is a major active ingredient extracted from natural herbal medicines, which has anti-inflammatory and strong anti-oxidation properties. In this study we investigated the effect of baicalin on P2Y12 receptor in the cervical DRG SGC-mediated sympathoexcitatory reflex, which is increased during MI. The results showed that the expression of P2Y12 receptor mRNA and protein in DRG, and the co-localization values of P2Y12 receptor and glial fibrillary acidic protein (GFAP) in cDRG SGCs were increased after MI. The activated SGCs increased IL-1β protein expression and elevated Akt phosphorylation in cDRG. Baicalin treatment inhibited the upregulation of the P2Y12 receptor, GFAP protein and Akt phosphorylation in cDRG neurons/SGCs. The stellate ganglia (SG) affect cardiac sympathetic activity. Baicalin treatment also decreased the upregulation of the P2Y12 receptor, GFAP protein in the SG. The P2Y12 agonist, 2Me-SADP, increased [Ca2+]i in HEK293 cells transfected with the P2Y12 receptor plasmid and SGCs in cDRG. These results indicate that application of baicalin alleviates pathologic sympathetic activity induced by MI via inhibition of afferents in the cDRG.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。