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

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 car...

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Main Authors: 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
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-07-01
Series:Frontiers in Physiology
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Online Access:https://www.frontiersin.org/article/10.3389/fphys.2018.00928/full
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author Lifang Zou
Lifang Zou
Xinyao Han
Shuangmei Liu
Shuangmei Liu
Yingxin Gong
Bing Wu
Bing Wu
Zhihua Yi
Zhihua Yi
Hui Liu
Hui Liu
Shanhong Zhao
Shanhong Zhao
Tianyu Jia
Tianyu Jia
Lin Li
Lin Li
Huilong Yuan
Huilong Yuan
Liran Shi
Liran Shi
Chunping Zhang
Chunping Zhang
Yun Gao
Yun Gao
Guilin Li
Guilin Li
Hong Xu
Hong Xu
Shangdong Liang
Shangdong Liang
spellingShingle Lifang Zou
Lifang Zou
Xinyao Han
Shuangmei Liu
Shuangmei Liu
Yingxin Gong
Bing Wu
Bing Wu
Zhihua Yi
Zhihua Yi
Hui Liu
Hui Liu
Shanhong Zhao
Shanhong Zhao
Tianyu Jia
Tianyu Jia
Lin Li
Lin Li
Huilong Yuan
Huilong Yuan
Liran Shi
Liran Shi
Chunping Zhang
Chunping Zhang
Yun Gao
Yun Gao
Guilin Li
Guilin Li
Hong Xu
Hong Xu
Shangdong Liang
Shangdong Liang
Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia
Frontiers in Physiology
P2Y12 receptor
dorsal root ganglia
satellite glial cells
myocardial ischemia
sympathoexcitatory reflex
author_facet Lifang Zou
Lifang Zou
Xinyao Han
Shuangmei Liu
Shuangmei Liu
Yingxin Gong
Bing Wu
Bing Wu
Zhihua Yi
Zhihua Yi
Hui Liu
Hui Liu
Shanhong Zhao
Shanhong Zhao
Tianyu Jia
Tianyu Jia
Lin Li
Lin Li
Huilong Yuan
Huilong Yuan
Liran Shi
Liran Shi
Chunping Zhang
Chunping Zhang
Yun Gao
Yun Gao
Guilin Li
Guilin Li
Hong Xu
Hong Xu
Shangdong Liang
Shangdong Liang
author_sort Lifang Zou
title Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia
title_short Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia
title_full Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia
title_fullStr Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia
title_full_unstemmed Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root Ganglia
title_sort baicalin depresses the sympathoexcitatory reflex induced by myocardial ischemia via the dorsal root ganglia
publisher Frontiers Media S.A.
series Frontiers in Physiology
issn 1664-042X
publishDate 2018-07-01
description 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.
topic P2Y12 receptor
dorsal root ganglia
satellite glial cells
myocardial ischemia
sympathoexcitatory reflex
url https://www.frontiersin.org/article/10.3389/fphys.2018.00928/full
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spelling doaj-2e4d1d751f764f6a89c39485c1094bb32020-11-24T23:10:18ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2018-07-01910.3389/fphys.2018.00928327541Baicalin Depresses the Sympathoexcitatory Reflex Induced by Myocardial Ischemia via the Dorsal Root GangliaLifang Zou0Lifang Zou1Xinyao Han2Shuangmei Liu3Shuangmei Liu4Yingxin Gong5Bing Wu6Bing Wu7Zhihua Yi8Zhihua Yi9Hui Liu10Hui Liu11Shanhong Zhao12Shanhong Zhao13Tianyu Jia14Tianyu Jia15Lin Li16Lin Li17Huilong Yuan18Huilong Yuan19Liran Shi20Liran Shi21Chunping Zhang22Chunping Zhang23Yun Gao24Yun Gao25Guilin Li26Guilin Li27Hong Xu28Hong Xu29Shangdong Liang30Shangdong Liang31Department of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaFirst Clinical Department, Medical School of Nanchang University, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaFirst Clinical Department, Medical School of Nanchang University, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Cell Biology, Medical School of Nanchang University, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaDepartment of Physiology, Medical School of Nanchang University, Nanchang, ChinaJiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, ChinaMyocardial 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.https://www.frontiersin.org/article/10.3389/fphys.2018.00928/fullP2Y12 receptordorsal root gangliasatellite glial cellsmyocardial ischemiasympathoexcitatory reflex