Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis

Glaesserella parasuis can induce endothelial barrier damage in piglets, although the mechanism by which this pathogen triggers inflammatory damage remains unclear. Baicalin possesses anti-inflammatory and anti-oxidant activities. However, whether baicalin can relieve endothelial barrier damage cause...

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Main Authors: Shulin Fu, Xinyue Tian, Chun Peng, Dan Zhang, Linglu Zhou, Yuzhen Yuan, Jing He, Ling Guo, Yinsheng Qiu, Chun Ye, Yu Liu, Bingbing Zong
Format: Article
Language:English
Published: Elsevier 2024-01-01
Series:Heliyon
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2405844023108401
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author Shulin Fu
Xinyue Tian
Chun Peng
Dan Zhang
Linglu Zhou
Yuzhen Yuan
Jing He
Ling Guo
Yinsheng Qiu
Chun Ye
Yu Liu
Bingbing Zong
author_facet Shulin Fu
Xinyue Tian
Chun Peng
Dan Zhang
Linglu Zhou
Yuzhen Yuan
Jing He
Ling Guo
Yinsheng Qiu
Chun Ye
Yu Liu
Bingbing Zong
author_sort Shulin Fu
collection DOAJ
description Glaesserella parasuis can induce endothelial barrier damage in piglets, although the mechanism by which this pathogen triggers inflammatory damage remains unclear. Baicalin possesses anti-inflammatory and anti-oxidant activities. However, whether baicalin can relieve endothelial barrier damage caused by Glaesserella parasuis infection has not yet been studied. Hence, we evaluated the ability of baicalin to counteract the changes induced by Glaesserella parasuis in porcine aortic vascular endothelial cells. The results showed that Glaesserella parasuis could upregulate the expression of pannexin 1 channel protein and promote the release of adenosine triphosphate, adenosine diphosphate, adenosine 3′-monophosphate, uridine triphosphate, uridine diphosphate, and uridine monophosphate in porcine aortic vascular endothelial cells. The expression level of purinergic receptor P2Y6 was upregulated in porcine aortic vascular endothelial cells triggered by Glaesserella parasuis. In addition, Glaesserella parasuis could activate phospholipase C-protein kinase C and myosin light chain kinase-myosin light chain signaling pathways in porcine aortic vascular endothelial cells. Baicalin could inhibit pannexin 1 channel protein expression, reduce adenosine triphosphate, adenosine diphosphate, adenosine 3′-monophosphate, uridine triphosphate, uridine diphosphate, and uridine monophosphate release, and attenuate the expression level of P2Y6 in porcine aortic vascular endothelial cells induced by Glaesserella parasuis. Baicalin could also reduce the activation of phospholipase C-protein kinase C and myosin light chain kinase-myosin light chain signaling pathways in porcine aortic vascular endothelial cells triggered by Glaesserella parasuis. Our study report that Glaesserella parasuis could promote pannexin 1 channel protein expression, induce nucleosides substance release, and P2Y6 expression in porcine aortic vascular endothelial cells and baicalin could inhibit the expression levels of pannexin 1, nucleosides substance, and P2Y6 in the porcine aortic vascular endothelial cells induced by Glaesserella parasuis, which might be served as some targets for treatment of inflammation disease caused by Glaesserella parasuis.
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spelling doaj.art-be550e08ab27425bba2aaf342fd873392024-02-01T06:32:42ZengElsevierHeliyon2405-84402024-01-01101e23632Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuisShulin Fu0Xinyue Tian1Chun Peng2Dan Zhang3Linglu Zhou4Yuzhen Yuan5Jing He6Ling Guo7Yinsheng Qiu8Chun Ye9Yu Liu10Bingbing Zong11Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR China; Corresponding author.Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China.Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaHubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, PR China; Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, PR ChinaGlaesserella parasuis can induce endothelial barrier damage in piglets, although the mechanism by which this pathogen triggers inflammatory damage remains unclear. Baicalin possesses anti-inflammatory and anti-oxidant activities. However, whether baicalin can relieve endothelial barrier damage caused by Glaesserella parasuis infection has not yet been studied. Hence, we evaluated the ability of baicalin to counteract the changes induced by Glaesserella parasuis in porcine aortic vascular endothelial cells. The results showed that Glaesserella parasuis could upregulate the expression of pannexin 1 channel protein and promote the release of adenosine triphosphate, adenosine diphosphate, adenosine 3′-monophosphate, uridine triphosphate, uridine diphosphate, and uridine monophosphate in porcine aortic vascular endothelial cells. The expression level of purinergic receptor P2Y6 was upregulated in porcine aortic vascular endothelial cells triggered by Glaesserella parasuis. In addition, Glaesserella parasuis could activate phospholipase C-protein kinase C and myosin light chain kinase-myosin light chain signaling pathways in porcine aortic vascular endothelial cells. Baicalin could inhibit pannexin 1 channel protein expression, reduce adenosine triphosphate, adenosine diphosphate, adenosine 3′-monophosphate, uridine triphosphate, uridine diphosphate, and uridine monophosphate release, and attenuate the expression level of P2Y6 in porcine aortic vascular endothelial cells induced by Glaesserella parasuis. Baicalin could also reduce the activation of phospholipase C-protein kinase C and myosin light chain kinase-myosin light chain signaling pathways in porcine aortic vascular endothelial cells triggered by Glaesserella parasuis. Our study report that Glaesserella parasuis could promote pannexin 1 channel protein expression, induce nucleosides substance release, and P2Y6 expression in porcine aortic vascular endothelial cells and baicalin could inhibit the expression levels of pannexin 1, nucleosides substance, and P2Y6 in the porcine aortic vascular endothelial cells induced by Glaesserella parasuis, which might be served as some targets for treatment of inflammation disease caused by Glaesserella parasuis.http://www.sciencedirect.com/science/article/pii/S2405844023108401Glaesserella parasuisBaicalinPannexin 1Liquid chromatography–tandem mass spectrometryP2Y6Phospholipase C-Protein kinase C
spellingShingle Shulin Fu
Xinyue Tian
Chun Peng
Dan Zhang
Linglu Zhou
Yuzhen Yuan
Jing He
Ling Guo
Yinsheng Qiu
Chun Ye
Yu Liu
Bingbing Zong
Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis
Heliyon
Glaesserella parasuis
Baicalin
Pannexin 1
Liquid chromatography–tandem mass spectrometry
P2Y6
Phospholipase C-Protein kinase C
title Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis
title_full Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis
title_fullStr Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis
title_full_unstemmed Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis
title_short Baicalin inhibited PANX-1/P2Y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by Glaesserella parasuis
title_sort baicalin inhibited panx 1 p2y6 signaling pathway activation in porcine aortic vascular endothelial cells infected by glaesserella parasuis
topic Glaesserella parasuis
Baicalin
Pannexin 1
Liquid chromatography–tandem mass spectrometry
P2Y6
Phospholipase C-Protein kinase C
url http://www.sciencedirect.com/science/article/pii/S2405844023108401
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