Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo

The increased vascular inflammation is a key event in the development of atherosclerotic lesions. Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing inflammation. However, the potential role of A. cinnamomea in cardiovascular diseases remains unexplored. Herei...

Full description

Bibliographic Details
Main Authors: Yan Zhang, Aijin Ma, Hao Xi, Ning Chen, Rong Wang, Chenhui Yang, Jinbang Chen, Pin Lv, Fuping Zheng, Wenyi Kang
Format: Article
Language:English
Published: KeAi Communications Co., Ltd. 2021-07-01
Series:Food Science and Human Wellness
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2213453021000513
id doaj-59ee2dab804d4127894dfce3621e8665
record_format Article
spelling doaj-59ee2dab804d4127894dfce3621e86652021-06-07T06:51:57ZengKeAi Communications Co., Ltd.Food Science and Human Wellness2213-45302021-07-01104421430Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivoYan Zhang0Aijin Ma1Hao Xi2Ning Chen3Rong Wang4Chenhui Yang5Jinbang Chen6Pin Lv7Fuping Zheng8Wenyi Kang9Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, Beijing 100048, China; Cardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, China; Hebei Food Safety Key Laboratory, Hebei Food Inspection and Research Institute, Shijiazhuang 050091, ChinaBeijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, Beijing 100048, ChinaCardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, ChinaCardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, ChinaCardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, ChinaCardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, ChinaCardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, ChinaBeijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, Beijing 100048, China; Cardiovascular Medical Science Center, Department of Cell Biology, Hebei Medical University, Shijiazhuang 050091, China; Corresponding author.Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, Beijing 100048, China; Corresponding author.National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng, Henan 475004, China; Corresponding author.The increased vascular inflammation is a key event in the development of atherosclerotic lesions. Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing inflammation. However, the potential role of A. cinnamomea in cardiovascular diseases remains unexplored. Herein, using carotid arterial ligation models, we found that ethanol extract from A. cinnamomea (EEAC) significantly inhibited neointimal hyperplasia in a dose-dependent manner, accompanied with the reduced expression of activated p65 and inflammatory cytokines. We also show that EEAC ameliorated TNF-α-induced phosphorylation of p65 and pro-inflammatory cytokine expression in both vascular smooth muscle cells (VSMCs) and macrophages in vitro. Mechanistically, EEAC suppressed expression levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM-1) in VSMCs, which attenuates the ability of monocytes/macrophages adhesion to VSMCs. Furthermore, the expression level of these adhesion molecules and infiltration of monocytes/macrophages were also decreased in neointimal VSMCs of arteries pretreated with EEAC. Altogether, our results reveal a novel function of A. cinnamomea in suppressing vascular inflammation upon ligation injury during neointimal formation, likely through inhibition of inflammatory cell infiltration via downregulating the adhesion molecules in VSMCs. Thus, A. cinnamomea may offer a pharmacological therapy to slow down disease progression in patients with vascular injury.http://www.sciencedirect.com/science/article/pii/S2213453021000513Antrodia cinnamomeaVascular smooth muscle cellsInflammationAdhesion moleculeNeointimal hyperplasia.
collection DOAJ
language English
format Article
sources DOAJ
author Yan Zhang
Aijin Ma
Hao Xi
Ning Chen
Rong Wang
Chenhui Yang
Jinbang Chen
Pin Lv
Fuping Zheng
Wenyi Kang
spellingShingle Yan Zhang
Aijin Ma
Hao Xi
Ning Chen
Rong Wang
Chenhui Yang
Jinbang Chen
Pin Lv
Fuping Zheng
Wenyi Kang
Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
Food Science and Human Wellness
Antrodia cinnamomea
Vascular smooth muscle cells
Inflammation
Adhesion molecule
Neointimal hyperplasia.
author_facet Yan Zhang
Aijin Ma
Hao Xi
Ning Chen
Rong Wang
Chenhui Yang
Jinbang Chen
Pin Lv
Fuping Zheng
Wenyi Kang
author_sort Yan Zhang
title Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
title_short Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
title_full Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
title_fullStr Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
title_full_unstemmed Antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
title_sort antrodia cinnamomea ameliorates neointimal formation by inhibiting inflammatory cell infiltration through downregulation of adhesion molecule expression in vitro and in vivo
publisher KeAi Communications Co., Ltd.
series Food Science and Human Wellness
issn 2213-4530
publishDate 2021-07-01
description The increased vascular inflammation is a key event in the development of atherosclerotic lesions. Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing inflammation. However, the potential role of A. cinnamomea in cardiovascular diseases remains unexplored. Herein, using carotid arterial ligation models, we found that ethanol extract from A. cinnamomea (EEAC) significantly inhibited neointimal hyperplasia in a dose-dependent manner, accompanied with the reduced expression of activated p65 and inflammatory cytokines. We also show that EEAC ameliorated TNF-α-induced phosphorylation of p65 and pro-inflammatory cytokine expression in both vascular smooth muscle cells (VSMCs) and macrophages in vitro. Mechanistically, EEAC suppressed expression levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM-1) in VSMCs, which attenuates the ability of monocytes/macrophages adhesion to VSMCs. Furthermore, the expression level of these adhesion molecules and infiltration of monocytes/macrophages were also decreased in neointimal VSMCs of arteries pretreated with EEAC. Altogether, our results reveal a novel function of A. cinnamomea in suppressing vascular inflammation upon ligation injury during neointimal formation, likely through inhibition of inflammatory cell infiltration via downregulating the adhesion molecules in VSMCs. Thus, A. cinnamomea may offer a pharmacological therapy to slow down disease progression in patients with vascular injury.
topic Antrodia cinnamomea
Vascular smooth muscle cells
Inflammation
Adhesion molecule
Neointimal hyperplasia.
url http://www.sciencedirect.com/science/article/pii/S2213453021000513
work_keys_str_mv AT yanzhang antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT aijinma antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT haoxi antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT ningchen antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT rongwang antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT chenhuiyang antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT jinbangchen antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT pinlv antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT fupingzheng antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
AT wenyikang antrodiacinnamomeaamelioratesneointimalformationbyinhibitinginflammatorycellinfiltrationthroughdownregulationofadhesionmoleculeexpressioninvitroandinvivo
_version_ 1721392174026719232