Biochanin A inhibits endothelial dysfunction induced by IL-6-stimulated endothelial microparticles in Perthes disease via the NF[kappa]B pathway

Endothelial dysfunction caused by the stimulation of endothelial microparticles (EMPs) by the inflammatory factor IL-6 is one of the pathogenic pathways associated with Perthes disease. The natural active product biochanin A (BCA) has an anti-inflammatory effect; however, whether it can alleviate en...

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Published in:Experimental and therapeutic medicine 2024-04, Vol.27 (4)
Main Authors: Liu, Jianhong, Lin, Chengsen, Li, Boxiang, Huang, Qian, Chen, Xianxiang, Tang, Shengping, Luo, Xiaolin, Lu, Rongbin, Liu, Yun, Liao, Shijie, Ding, Xiaofei
Format: Article
Language:English
Subjects:
Care and treatment
Complications and side effects
Development and progression
Health aspects
Interleukin-6
Isoflavones
Legg-Calve-Perthes disease
Physiological aspects
Vascular endothelium
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container_title Experimental and therapeutic medicine
container_volume 27
creator Liu, Jianhong
Lin, Chengsen
Li, Boxiang
Huang, Qian
Chen, Xianxiang
Tang, Shengping
Luo, Xiaolin
Lu, Rongbin
Liu, Yun
Liao, Shijie
Ding, Xiaofei
description Endothelial dysfunction caused by the stimulation of endothelial microparticles (EMPs) by the inflammatory factor IL-6 is one of the pathogenic pathways associated with Perthes disease. The natural active product biochanin A (BCA) has an anti-inflammatory effect; however, whether it can alleviate endothelial dysfunction in Perthes disease is not known. The present in vitro experiments on human umbilical vein endothelial cells showed that 0-100 pg/ml IL-6-EMPs could induce endothelial dysfunction in a concentration-dependent manner, and the results of the Cell Counting Kit 8 assay revealed that, at concentrations of
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The natural active product biochanin A (BCA) has an anti-inflammatory effect; however, whether it can alleviate endothelial dysfunction in Perthes disease is not known. The present in vitro experiments on human umbilical vein endothelial cells showed that 0-100 pg/ml IL-6-EMPs could induce endothelial dysfunction in a concentration-dependent manner, and the results of the Cell Counting Kit 8 assay revealed that, at concentrations of &lt;20 [micro]M, BCA had no cytotoxic effect. Reverse transcription-quantitative PCR demonstrated that BCA reduced the expression levels of the endothelial dysfunction indexes E-selectin and intercellular cell adhesion molecule-1 (ICAM-1) in a concentration-dependent manner. Immunofluorescence and western blotting illustrated that BCA increased the expression levels of zonula occludens-1 and decreased those of ICAM-1. Mechanistic studies showed that BCA inhibited activation of the NF[kappa]B pathway. In vivo experiments demonstrated that IL-6 was significantly increased in the rat model of ischemic necrosis of the femoral head, whereas BCA inhibited IL-6 production. Therefore, in Perthes disease, BCA may inhibit the NF[kappa]B pathway to suppress IL-6-EMP-induced endothelial dysfunction, and could thus be regarded as a potential treatment for Perthes disease. Key words: Perthes disease, biochanin A, NF[kappa]B signaling pathway, IL-6, endothelial microparticles, endothelial dysfunction</description><identifier>ISSN: 1792-0981</identifier><identifier>DOI: 10.3892/etm.2024.12425</identifier><language>eng</language><publisher>Spandidos Publications</publisher><subject>Care and treatment ; Complications and side effects ; Development and progression ; Health aspects ; Interleukin-6 ; Isoflavones ; Legg-Calve-Perthes disease ; Physiological aspects ; Vascular endothelium</subject><ispartof>Experimental and therapeutic medicine, 2024-04, Vol.27 (4)</ispartof><rights>COPYRIGHT 2024 Spandidos Publications</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids></links><search><creatorcontrib>Liu, Jianhong</creatorcontrib><creatorcontrib>Lin, Chengsen</creatorcontrib><creatorcontrib>Li, Boxiang</creatorcontrib><creatorcontrib>Huang, Qian</creatorcontrib><creatorcontrib>Chen, Xianxiang</creatorcontrib><creatorcontrib>Tang, Shengping</creatorcontrib><creatorcontrib>Luo, Xiaolin</creatorcontrib><creatorcontrib>Lu, Rongbin</creatorcontrib><creatorcontrib>Liu, Yun</creatorcontrib><creatorcontrib>Liao, Shijie</creatorcontrib><creatorcontrib>Ding, Xiaofei</creatorcontrib><title>Biochanin A inhibits endothelial dysfunction induced by IL-6-stimulated endothelial microparticles in Perthes disease via the NF[kappa]B pathway</title><title>Experimental and therapeutic medicine</title><description>Endothelial dysfunction caused by the stimulation of endothelial microparticles (EMPs) by the inflammatory factor IL-6 is one of the pathogenic pathways associated with Perthes disease. The natural active product biochanin A (BCA) has an anti-inflammatory effect; however, whether it can alleviate endothelial dysfunction in Perthes disease is not known. The present in vitro experiments on human umbilical vein endothelial cells showed that 0-100 pg/ml IL-6-EMPs could induce endothelial dysfunction in a concentration-dependent manner, and the results of the Cell Counting Kit 8 assay revealed that, at concentrations of &lt;20 [micro]M, BCA had no cytotoxic effect. Reverse transcription-quantitative PCR demonstrated that BCA reduced the expression levels of the endothelial dysfunction indexes E-selectin and intercellular cell adhesion molecule-1 (ICAM-1) in a concentration-dependent manner. Immunofluorescence and western blotting illustrated that BCA increased the expression levels of zonula occludens-1 and decreased those of ICAM-1. Mechanistic studies showed that BCA inhibited activation of the NF[kappa]B pathway. In vivo experiments demonstrated that IL-6 was significantly increased in the rat model of ischemic necrosis of the femoral head, whereas BCA inhibited IL-6 production. Therefore, in Perthes disease, BCA may inhibit the NF[kappa]B pathway to suppress IL-6-EMP-induced endothelial dysfunction, and could thus be regarded as a potential treatment for Perthes disease. 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The natural active product biochanin A (BCA) has an anti-inflammatory effect; however, whether it can alleviate endothelial dysfunction in Perthes disease is not known. The present in vitro experiments on human umbilical vein endothelial cells showed that 0-100 pg/ml IL-6-EMPs could induce endothelial dysfunction in a concentration-dependent manner, and the results of the Cell Counting Kit 8 assay revealed that, at concentrations of &lt;20 [micro]M, BCA had no cytotoxic effect. Reverse transcription-quantitative PCR demonstrated that BCA reduced the expression levels of the endothelial dysfunction indexes E-selectin and intercellular cell adhesion molecule-1 (ICAM-1) in a concentration-dependent manner. Immunofluorescence and western blotting illustrated that BCA increased the expression levels of zonula occludens-1 and decreased those of ICAM-1. Mechanistic studies showed that BCA inhibited activation of the NF[kappa]B pathway. In vivo experiments demonstrated that IL-6 was significantly increased in the rat model of ischemic necrosis of the femoral head, whereas BCA inhibited IL-6 production. Therefore, in Perthes disease, BCA may inhibit the NF[kappa]B pathway to suppress IL-6-EMP-induced endothelial dysfunction, and could thus be regarded as a potential treatment for Perthes disease. Key words: Perthes disease, biochanin A, NF[kappa]B signaling pathway, IL-6, endothelial microparticles, endothelial dysfunction</abstract><pub>Spandidos Publications</pub><doi>10.3892/etm.2024.12425</doi></addata></record>
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subjects Care and treatment
Complications and side effects
Development and progression
Health aspects
Interleukin-6
Isoflavones
Legg-Calve-Perthes disease
Physiological aspects
Vascular endothelium
title Biochanin A inhibits endothelial dysfunction induced by IL-6-stimulated endothelial microparticles in Perthes disease via the NF[kappa]B pathway
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