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Anti-atherogenic mechanism of ethanol extract of Christia vespertilionis (L.f.) Bakh. F. Leaves in vitro
[Display omitted] •CV extract attenuates monocyte adhesion to activated endothelial cells.•CV extract inhibits expression of adhesion molecules expression and chemokines.•CV extract inhibits NF-κB signaling pathway. Vascular inflammation is the key event in early atherogenesis. Pro-inflammatory endo...
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Published in: | International immunopharmacology 2024-06, Vol.134, p.112148, Article 112148 |
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•CV extract attenuates monocyte adhesion to activated endothelial cells.•CV extract inhibits expression of adhesion molecules expression and chemokines.•CV extract inhibits NF-κB signaling pathway.
Vascular inflammation is the key event in early atherogenesis. Pro-inflammatory endothelial cells induce monocyte recruitment into the sub-endothelial layer of the artery. This requires endothelial expression of adhesion molecules namely intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), alongside chemokines production. Christia vespertilionis (L.f.) Bakh.f. (CV) possesses anti-inflammatory property. However, its potential anti-atherogenic effect in the context of vascular inflammation has yet to be explored.
To evaluate the anti-atherogenic mechanism of 80% ethanol extract of CV leaves on tumor necrosis factor-α (TNF-α)-activated human umbilical vein endothelial cells (HUVECs).
Qualitative analysis of the CV extract was carried out by using liquid chromatography with tandem mass spectrometry (LC-MS/MS). The cell viability of HUVECs treated with CV extract was determined by MTT assay. The effect of CV extract on monocyte adhesion was determined by monocyte-endothelial adhesion assay. Protein expressions of ICAM-1, VCAM-1 and nuclear factor-kappa B (NF-κB) signaling pathway were determined by western blot while production of monocyte chemoattractant protein-1 (MCP-1) was determined by ELISA.
LC-MS/MS analysis showed that CV extract composed of five main compounds, including schaftoside, orientin, isovitexin, 6-caffeoyl-D-glucose, and 3,3′-di-O-methyl ellagic acid. Treatment of CV extract at a concentration range from 5 to 60 µg/mL for 24 h maintained HUVECs viability above 90 %, therefore concentrations of 20, 40 and 60 μg/mL were selected for the subsequent experiments. All concentrations of CV extract showed a significant inhibitory effect on monocyte adhesion to TNF-α-activated HUVECs (p |
doi_str_mv | 10.1016/j.intimp.2024.112148 |
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•CV extract attenuates monocyte adhesion to activated endothelial cells.•CV extract inhibits expression of adhesion molecules expression and chemokines.•CV extract inhibits NF-κB signaling pathway.
Vascular inflammation is the key event in early atherogenesis. Pro-inflammatory endothelial cells induce monocyte recruitment into the sub-endothelial layer of the artery. This requires endothelial expression of adhesion molecules namely intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), alongside chemokines production. Christia vespertilionis (L.f.) Bakh.f. (CV) possesses anti-inflammatory property. However, its potential anti-atherogenic effect in the context of vascular inflammation has yet to be explored.
To evaluate the anti-atherogenic mechanism of 80% ethanol extract of CV leaves on tumor necrosis factor-α (TNF-α)-activated human umbilical vein endothelial cells (HUVECs).
Qualitative analysis of the CV extract was carried out by using liquid chromatography with tandem mass spectrometry (LC-MS/MS). The cell viability of HUVECs treated with CV extract was determined by MTT assay. The effect of CV extract on monocyte adhesion was determined by monocyte-endothelial adhesion assay. Protein expressions of ICAM-1, VCAM-1 and nuclear factor-kappa B (NF-κB) signaling pathway were determined by western blot while production of monocyte chemoattractant protein-1 (MCP-1) was determined by ELISA.
LC-MS/MS analysis showed that CV extract composed of five main compounds, including schaftoside, orientin, isovitexin, 6-caffeoyl-D-glucose, and 3,3′-di-O-methyl ellagic acid. Treatment of CV extract at a concentration range from 5 to 60 µg/mL for 24 h maintained HUVECs viability above 90 %, therefore concentrations of 20, 40 and 60 μg/mL were selected for the subsequent experiments. All concentrations of CV extract showed a significant inhibitory effect on monocyte adhesion to TNF-α-activated HUVECs (p < 0.05). In addition, the protein expressions of ICAM-1 and VCAM-1 were significantly attenuated by CV in a concentration dependent manner (p < 0.001). At all tested concentrations, CV extract also exhibited significant inhibition on the production of MCP-1 (p < 0.05). Moreover, CV extract significantly inhibited TNF-α-induced phosphorylation of inhibitor of nuclear factor-κB kinase alpha/beta (IKKα/β), inhibitor kappa B-alpha (IκBα), NF-κB and nuclear translocation of NF-κB (p < 0.05).
CV extract inhibited monocyte adhesion to endothelial cells by suppressing protein expressions of cell adhesion molecules and production of chemokines through downregulation of NF-κB signaling pathway. Thus, CV has the potential to be developed as an anti-atherogenic agent for early treatment of atherosclerosis.</description><identifier>ISSN: 1567-5769</identifier><identifier>ISSN: 1878-1705</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2024.112148</identifier><identifier>PMID: 38718657</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Anti-inflammatory ; Atherosclerosis ; Christia vespertilionis ; Endothelial cell ; Monocyte adhesion ; NF-κB signaling pathway</subject><ispartof>International immunopharmacology, 2024-06, Vol.134, p.112148, Article 112148</ispartof><rights>2024 Elsevier B.V.</rights><rights>Copyright © 2024 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c311t-474dd979a131656f540cd565727dc7de6823f20bd02a83a13202bfcaaccf8a823</cites><orcidid>0000-0001-9066-4780</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38718657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tan, Jiah Ning</creatorcontrib><creatorcontrib>Husain, Khairana</creatorcontrib><creatorcontrib>Jubri, Zakiah</creatorcontrib><creatorcontrib>Chan, Kok Meng</creatorcontrib><creatorcontrib>Ugusman, Azizah</creatorcontrib><creatorcontrib>Jantan, Ibrahim</creatorcontrib><creatorcontrib>Fauzi, Norsyahida Mohd</creatorcontrib><title>Anti-atherogenic mechanism of ethanol extract of Christia vespertilionis (L.f.) Bakh. F. Leaves in vitro</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>[Display omitted]
•CV extract attenuates monocyte adhesion to activated endothelial cells.•CV extract inhibits expression of adhesion molecules expression and chemokines.•CV extract inhibits NF-κB signaling pathway.
Vascular inflammation is the key event in early atherogenesis. Pro-inflammatory endothelial cells induce monocyte recruitment into the sub-endothelial layer of the artery. This requires endothelial expression of adhesion molecules namely intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), alongside chemokines production. Christia vespertilionis (L.f.) Bakh.f. (CV) possesses anti-inflammatory property. However, its potential anti-atherogenic effect in the context of vascular inflammation has yet to be explored.
To evaluate the anti-atherogenic mechanism of 80% ethanol extract of CV leaves on tumor necrosis factor-α (TNF-α)-activated human umbilical vein endothelial cells (HUVECs).
Qualitative analysis of the CV extract was carried out by using liquid chromatography with tandem mass spectrometry (LC-MS/MS). The cell viability of HUVECs treated with CV extract was determined by MTT assay. The effect of CV extract on monocyte adhesion was determined by monocyte-endothelial adhesion assay. Protein expressions of ICAM-1, VCAM-1 and nuclear factor-kappa B (NF-κB) signaling pathway were determined by western blot while production of monocyte chemoattractant protein-1 (MCP-1) was determined by ELISA.
LC-MS/MS analysis showed that CV extract composed of five main compounds, including schaftoside, orientin, isovitexin, 6-caffeoyl-D-glucose, and 3,3′-di-O-methyl ellagic acid. Treatment of CV extract at a concentration range from 5 to 60 µg/mL for 24 h maintained HUVECs viability above 90 %, therefore concentrations of 20, 40 and 60 μg/mL were selected for the subsequent experiments. All concentrations of CV extract showed a significant inhibitory effect on monocyte adhesion to TNF-α-activated HUVECs (p < 0.05). In addition, the protein expressions of ICAM-1 and VCAM-1 were significantly attenuated by CV in a concentration dependent manner (p < 0.001). At all tested concentrations, CV extract also exhibited significant inhibition on the production of MCP-1 (p < 0.05). Moreover, CV extract significantly inhibited TNF-α-induced phosphorylation of inhibitor of nuclear factor-κB kinase alpha/beta (IKKα/β), inhibitor kappa B-alpha (IκBα), NF-κB and nuclear translocation of NF-κB (p < 0.05).
CV extract inhibited monocyte adhesion to endothelial cells by suppressing protein expressions of cell adhesion molecules and production of chemokines through downregulation of NF-κB signaling pathway. Thus, CV has the potential to be developed as an anti-atherogenic agent for early treatment of atherosclerosis.</description><subject>Anti-inflammatory</subject><subject>Atherosclerosis</subject><subject>Christia vespertilionis</subject><subject>Endothelial cell</subject><subject>Monocyte adhesion</subject><subject>NF-κB signaling pathway</subject><issn>1567-5769</issn><issn>1878-1705</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kMtOxCAUQInROL7-wBiWumiFthRmY6ITX8kkbnRNGLi1jG0ZgZno38uko0tX3FzOfR2EzinJKaH19TK3Q7T9Ki9IUeWUFrQSe-iICi4yygnbTzGrecZ4PZ2g4xCWhKR8RQ_RpBSciprxI9TepiaZii149w6D1bgH3arBhh67BkNMseswfEWvdNymZq23IVqFNxBW4KPtrEs4vpznTX6F79RHm-OHHM9BJQLbAW9s9O4UHTSqC3C2e0_Q28P96-wpm788Ps9u55kuKY1ZxStjpnyqaElrVjesItqwtGrBjeYGalGUTUEWhhRKlIlK1y8arZTWjVDp8wRdjn1X3n2uIUTZ26Ch69QAbh1kSVhJS0EKltBqRLV3IXho5MrbXvlvSYncOpZLOTqWW8dydJzKLnYT1osezF_Rr9QE3IwApDs3FrwM2sKgwVgPOkrj7P8TfgCgiI5_</recordid><startdate>20240615</startdate><enddate>20240615</enddate><creator>Tan, Jiah Ning</creator><creator>Husain, Khairana</creator><creator>Jubri, Zakiah</creator><creator>Chan, Kok Meng</creator><creator>Ugusman, Azizah</creator><creator>Jantan, Ibrahim</creator><creator>Fauzi, Norsyahida Mohd</creator><general>Elsevier B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9066-4780</orcidid></search><sort><creationdate>20240615</creationdate><title>Anti-atherogenic mechanism of ethanol extract of Christia vespertilionis (L.f.) Bakh. F. Leaves in vitro</title><author>Tan, Jiah Ning ; Husain, Khairana ; Jubri, Zakiah ; Chan, Kok Meng ; Ugusman, Azizah ; Jantan, Ibrahim ; Fauzi, Norsyahida Mohd</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-474dd979a131656f540cd565727dc7de6823f20bd02a83a13202bfcaaccf8a823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Anti-inflammatory</topic><topic>Atherosclerosis</topic><topic>Christia vespertilionis</topic><topic>Endothelial cell</topic><topic>Monocyte adhesion</topic><topic>NF-κB signaling pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tan, Jiah Ning</creatorcontrib><creatorcontrib>Husain, Khairana</creatorcontrib><creatorcontrib>Jubri, Zakiah</creatorcontrib><creatorcontrib>Chan, Kok Meng</creatorcontrib><creatorcontrib>Ugusman, Azizah</creatorcontrib><creatorcontrib>Jantan, Ibrahim</creatorcontrib><creatorcontrib>Fauzi, Norsyahida Mohd</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tan, Jiah Ning</au><au>Husain, Khairana</au><au>Jubri, Zakiah</au><au>Chan, Kok Meng</au><au>Ugusman, Azizah</au><au>Jantan, Ibrahim</au><au>Fauzi, Norsyahida Mohd</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-atherogenic mechanism of ethanol extract of Christia vespertilionis (L.f.) Bakh. F. Leaves in vitro</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2024-06-15</date><risdate>2024</risdate><volume>134</volume><spage>112148</spage><pages>112148-</pages><artnum>112148</artnum><issn>1567-5769</issn><issn>1878-1705</issn><eissn>1878-1705</eissn><abstract>[Display omitted]
•CV extract attenuates monocyte adhesion to activated endothelial cells.•CV extract inhibits expression of adhesion molecules expression and chemokines.•CV extract inhibits NF-κB signaling pathway.
Vascular inflammation is the key event in early atherogenesis. Pro-inflammatory endothelial cells induce monocyte recruitment into the sub-endothelial layer of the artery. This requires endothelial expression of adhesion molecules namely intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), alongside chemokines production. Christia vespertilionis (L.f.) Bakh.f. (CV) possesses anti-inflammatory property. However, its potential anti-atherogenic effect in the context of vascular inflammation has yet to be explored.
To evaluate the anti-atherogenic mechanism of 80% ethanol extract of CV leaves on tumor necrosis factor-α (TNF-α)-activated human umbilical vein endothelial cells (HUVECs).
Qualitative analysis of the CV extract was carried out by using liquid chromatography with tandem mass spectrometry (LC-MS/MS). The cell viability of HUVECs treated with CV extract was determined by MTT assay. The effect of CV extract on monocyte adhesion was determined by monocyte-endothelial adhesion assay. Protein expressions of ICAM-1, VCAM-1 and nuclear factor-kappa B (NF-κB) signaling pathway were determined by western blot while production of monocyte chemoattractant protein-1 (MCP-1) was determined by ELISA.
LC-MS/MS analysis showed that CV extract composed of five main compounds, including schaftoside, orientin, isovitexin, 6-caffeoyl-D-glucose, and 3,3′-di-O-methyl ellagic acid. Treatment of CV extract at a concentration range from 5 to 60 µg/mL for 24 h maintained HUVECs viability above 90 %, therefore concentrations of 20, 40 and 60 μg/mL were selected for the subsequent experiments. All concentrations of CV extract showed a significant inhibitory effect on monocyte adhesion to TNF-α-activated HUVECs (p < 0.05). In addition, the protein expressions of ICAM-1 and VCAM-1 were significantly attenuated by CV in a concentration dependent manner (p < 0.001). At all tested concentrations, CV extract also exhibited significant inhibition on the production of MCP-1 (p < 0.05). Moreover, CV extract significantly inhibited TNF-α-induced phosphorylation of inhibitor of nuclear factor-κB kinase alpha/beta (IKKα/β), inhibitor kappa B-alpha (IκBα), NF-κB and nuclear translocation of NF-κB (p < 0.05).
CV extract inhibited monocyte adhesion to endothelial cells by suppressing protein expressions of cell adhesion molecules and production of chemokines through downregulation of NF-κB signaling pathway. Thus, CV has the potential to be developed as an anti-atherogenic agent for early treatment of atherosclerosis.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>38718657</pmid><doi>10.1016/j.intimp.2024.112148</doi><orcidid>https://orcid.org/0000-0001-9066-4780</orcidid></addata></record> |
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subjects | Anti-inflammatory Atherosclerosis Christia vespertilionis Endothelial cell Monocyte adhesion NF-κB signaling pathway |
title | Anti-atherogenic mechanism of ethanol extract of Christia vespertilionis (L.f.) Bakh. F. Leaves in vitro |
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