Active polypeptides from Hirudo inhibit endothelial cell inflammation and macrophage foam cell formation by regulating the LOX-1/LXR-α/ABCA1 pathway
[Display omitted] •HE (PP) inhibits adhesion and inflammatory response in endothelial cells.•HE (PP) suppresses foam cell formation and apoptosis in macrophages.•HE (PP) inhibits lipid accumulation by regulating LOX-1/LXR-α/ABCA1 pathway.•HE (PP) is identified as a potential novel therapy for athero...
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| Veröffentlicht in: | Biomedicine & pharmacotherapy 2019-07, Vol.115, p.108840-108840, Article 108840 |
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| creator | Lu, Jing Chen, Xuenan Xu, Xiaohao Liu, Jianzeng Zhang, Zepeng Wang, Mingxing Li, Xiangzhu Chen, Hong Zhao, Daqing Wang, Jian Zhao, Dexi Cong, Deyu Li, Xiangyan Sun, Liwei |
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•HE (PP) inhibits adhesion and inflammatory response in endothelial cells.•HE (PP) suppresses foam cell formation and apoptosis in macrophages.•HE (PP) inhibits lipid accumulation by regulating LOX-1/LXR-α/ABCA1 pathway.•HE (PP) is identified as a potential novel therapy for atherosclerosis prevention.
Hirudo is an important Chinese medicine that has been widely used in patients with thrombosis-related diseases. We aimed to evaluate the protective effect and potential mechanism of Hirudo extract (HE) on the process of atherosclerosis (AS) as well as identify its active components in the lipopolysaccharide (LPS) - or oxidized low-density lipoprotein (ox-LDL)-induced cell models.
After treatment, adhesion molecules and pro-inflammatory cytokines induced by LPS were examined by qPCR and ELISA. ROS production, cell apoptosis, and lipid accumulation in ox-LDL-induced cells were analyzed by flow cytometry, qPCR, western blotting, and immunofluorescence staining. In addition, the main active components of HE were identified and analyzed for preventing the progression of AS.
In this study, we found that HE pretreatment for 48 h significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Moreover, HE attenuated ox-LDL-induced ROS accumulation and apoptosis in macrophage cells via mitochondrial apoptotic pathways. Additionally, HE pretreatment effectively inhibited cholesterol uptake and increased cholesterol efflux by regulating the LOX-1/LXR-α/ABCA1 pathway. Importantly, the polypeptides from HE (PP) with a molecular weight |
| doi_str_mv | 10.1016/j.biopha.2019.108840 |
| format | Article |
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•HE (PP) inhibits adhesion and inflammatory response in endothelial cells.•HE (PP) suppresses foam cell formation and apoptosis in macrophages.•HE (PP) inhibits lipid accumulation by regulating LOX-1/LXR-α/ABCA1 pathway.•HE (PP) is identified as a potential novel therapy for atherosclerosis prevention.
Hirudo is an important Chinese medicine that has been widely used in patients with thrombosis-related diseases. We aimed to evaluate the protective effect and potential mechanism of Hirudo extract (HE) on the process of atherosclerosis (AS) as well as identify its active components in the lipopolysaccharide (LPS) - or oxidized low-density lipoprotein (ox-LDL)-induced cell models.
After treatment, adhesion molecules and pro-inflammatory cytokines induced by LPS were examined by qPCR and ELISA. ROS production, cell apoptosis, and lipid accumulation in ox-LDL-induced cells were analyzed by flow cytometry, qPCR, western blotting, and immunofluorescence staining. In addition, the main active components of HE were identified and analyzed for preventing the progression of AS.
In this study, we found that HE pretreatment for 48 h significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Moreover, HE attenuated ox-LDL-induced ROS accumulation and apoptosis in macrophage cells via mitochondrial apoptotic pathways. Additionally, HE pretreatment effectively inhibited cholesterol uptake and increased cholesterol efflux by regulating the LOX-1/LXR-α/ABCA1 pathway. Importantly, the polypeptides from HE (PP) with a molecular weight < 10,000 Da accounted for about 62.9% of the total amount of polypeptides, which in turn may be active components of HE that are responsible for inhibiting inflammation, foam cell formation and apoptosis.
PP from HE potently inhibits endothelial cell inflammatory injury and macrophage foam cell formation and apoptosis by regulating the LOX-1/LXR-α/ABCA1 pathway, thereby providing additional support to the beneficial effects of HE in preventing AS.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2019.108840</identifier><identifier>PMID: 31048189</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Animals ; ATP Binding Cassette Transporter 1 - genetics ; ATP Binding Cassette Transporter 1 - metabolism ; Cell Adhesion - drug effects ; Cholesterol - metabolism ; Cholesterol uptake and efflux ; Dose-Response Relationship, Drug ; Foam cell formation ; Foam Cells - drug effects ; Gene Expression Regulation - drug effects ; Hirudo extract ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Inflammation - drug therapy ; Inflammation - metabolism ; Inflammatory response ; Leeches - chemistry ; Lipopolysaccharides - administration & dosage ; Lipopolysaccharides - toxicity ; Lipoproteins, LDL - administration & dosage ; Lipoproteins, LDL - toxicity ; Liver X Receptors - genetics ; Liver X Receptors - metabolism ; Macrophages - drug effects ; Mice ; Peptides - chemistry ; Peptides - pharmacology ; Polypeptides ; RAW 264.7 Cells ; Reactive Oxygen Species ; Scavenger Receptors, Class E - genetics ; Scavenger Receptors, Class E - metabolism ; THP-1 Cells</subject><ispartof>Biomedicine & pharmacotherapy, 2019-07, Vol.115, p.108840-108840, Article 108840</ispartof><rights>2019 The Authors</rights><rights>Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-ea5f4d3a6a983d996c685a9bb38d8064124e0158ce7a5355bd52cce1e9ccc5cd3</citedby><cites>FETCH-LOGICAL-c408t-ea5f4d3a6a983d996c685a9bb38d8064124e0158ce7a5355bd52cce1e9ccc5cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.biopha.2019.108840$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31048189$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Jing</creatorcontrib><creatorcontrib>Chen, Xuenan</creatorcontrib><creatorcontrib>Xu, Xiaohao</creatorcontrib><creatorcontrib>Liu, Jianzeng</creatorcontrib><creatorcontrib>Zhang, Zepeng</creatorcontrib><creatorcontrib>Wang, Mingxing</creatorcontrib><creatorcontrib>Li, Xiangzhu</creatorcontrib><creatorcontrib>Chen, Hong</creatorcontrib><creatorcontrib>Zhao, Daqing</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Zhao, Dexi</creatorcontrib><creatorcontrib>Cong, Deyu</creatorcontrib><creatorcontrib>Li, Xiangyan</creatorcontrib><creatorcontrib>Sun, Liwei</creatorcontrib><title>Active polypeptides from Hirudo inhibit endothelial cell inflammation and macrophage foam cell formation by regulating the LOX-1/LXR-α/ABCA1 pathway</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>[Display omitted]
•HE (PP) inhibits adhesion and inflammatory response in endothelial cells.•HE (PP) suppresses foam cell formation and apoptosis in macrophages.•HE (PP) inhibits lipid accumulation by regulating LOX-1/LXR-α/ABCA1 pathway.•HE (PP) is identified as a potential novel therapy for atherosclerosis prevention.
Hirudo is an important Chinese medicine that has been widely used in patients with thrombosis-related diseases. We aimed to evaluate the protective effect and potential mechanism of Hirudo extract (HE) on the process of atherosclerosis (AS) as well as identify its active components in the lipopolysaccharide (LPS) - or oxidized low-density lipoprotein (ox-LDL)-induced cell models.
After treatment, adhesion molecules and pro-inflammatory cytokines induced by LPS were examined by qPCR and ELISA. ROS production, cell apoptosis, and lipid accumulation in ox-LDL-induced cells were analyzed by flow cytometry, qPCR, western blotting, and immunofluorescence staining. In addition, the main active components of HE were identified and analyzed for preventing the progression of AS.
In this study, we found that HE pretreatment for 48 h significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Moreover, HE attenuated ox-LDL-induced ROS accumulation and apoptosis in macrophage cells via mitochondrial apoptotic pathways. Additionally, HE pretreatment effectively inhibited cholesterol uptake and increased cholesterol efflux by regulating the LOX-1/LXR-α/ABCA1 pathway. Importantly, the polypeptides from HE (PP) with a molecular weight < 10,000 Da accounted for about 62.9% of the total amount of polypeptides, which in turn may be active components of HE that are responsible for inhibiting inflammation, foam cell formation and apoptosis.
PP from HE potently inhibits endothelial cell inflammatory injury and macrophage foam cell formation and apoptosis by regulating the LOX-1/LXR-α/ABCA1 pathway, thereby providing additional support to the beneficial effects of HE in preventing AS.</description><subject>Animals</subject><subject>ATP Binding Cassette Transporter 1 - genetics</subject><subject>ATP Binding Cassette Transporter 1 - metabolism</subject><subject>Cell Adhesion - drug effects</subject><subject>Cholesterol - metabolism</subject><subject>Cholesterol uptake and efflux</subject><subject>Dose-Response Relationship, Drug</subject><subject>Foam cell formation</subject><subject>Foam Cells - drug effects</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hirudo extract</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory response</subject><subject>Leeches - chemistry</subject><subject>Lipopolysaccharides - administration & dosage</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lipoproteins, LDL - administration & dosage</subject><subject>Lipoproteins, LDL - toxicity</subject><subject>Liver X Receptors - genetics</subject><subject>Liver X Receptors - metabolism</subject><subject>Macrophages - drug effects</subject><subject>Mice</subject><subject>Peptides - chemistry</subject><subject>Peptides - pharmacology</subject><subject>Polypeptides</subject><subject>RAW 264.7 Cells</subject><subject>Reactive Oxygen Species</subject><subject>Scavenger Receptors, Class E - genetics</subject><subject>Scavenger Receptors, Class E - metabolism</subject><subject>THP-1 Cells</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2O0zAUgC0EYsrADRDykk1a_8SpvUEqFcMgVRppNEizsxz7pXWVxMF2BvUgcxAuwplIlcKSlfX8vvenD6H3lCwpodXquKx9GA5myQhV05eUJXmBFlQJUlSErF-iBVkLXnDO2BV6k9KRECIqLl-jK05JKalUC_S8sdk_AR5CexpgyN5Bwk0MHb71cXQB-_7ga58x9C7kA7TetNhC206JpjVdZ7IPPTa9w52x8bzQHnATTDdTTYgXpD7hCPuxnaJ-j6dWeHf3WNDV7vG--P1rtfm83VA8mHz4aU5v0avGtAneXd5r9P3my8P2ttjdff223ewKWxKZCzCiKR03lVGSO6UqW0lhVF1z6SSpSspKIFRIC2sjuBC1E8xaoKCstcI6fo0-zn2HGH6MkLLufDrvbXoIY9KMMcXKsqJyQssZnY5MKUKjh-g7E0-aEn0Woo96FqLPQvQsZCr7cJkw1h24f0V_DUzApxmA6c4nD1En66G34HwEm7UL_v8T_gBP1KC2</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>Lu, Jing</creator><creator>Chen, Xuenan</creator><creator>Xu, Xiaohao</creator><creator>Liu, Jianzeng</creator><creator>Zhang, Zepeng</creator><creator>Wang, Mingxing</creator><creator>Li, Xiangzhu</creator><creator>Chen, Hong</creator><creator>Zhao, Daqing</creator><creator>Wang, Jian</creator><creator>Zhao, Dexi</creator><creator>Cong, Deyu</creator><creator>Li, Xiangyan</creator><creator>Sun, Liwei</creator><general>Elsevier Masson SAS</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201907</creationdate><title>Active polypeptides from Hirudo inhibit endothelial cell inflammation and macrophage foam cell formation by regulating the LOX-1/LXR-α/ABCA1 pathway</title><author>Lu, Jing ; Chen, Xuenan ; Xu, Xiaohao ; Liu, Jianzeng ; Zhang, Zepeng ; Wang, Mingxing ; Li, Xiangzhu ; Chen, Hong ; Zhao, Daqing ; Wang, Jian ; Zhao, Dexi ; Cong, Deyu ; Li, Xiangyan ; Sun, Liwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-ea5f4d3a6a983d996c685a9bb38d8064124e0158ce7a5355bd52cce1e9ccc5cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>ATP Binding Cassette Transporter 1 - genetics</topic><topic>ATP Binding Cassette Transporter 1 - metabolism</topic><topic>Cell Adhesion - drug effects</topic><topic>Cholesterol - metabolism</topic><topic>Cholesterol uptake and efflux</topic><topic>Dose-Response Relationship, Drug</topic><topic>Foam cell formation</topic><topic>Foam Cells - drug effects</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hirudo extract</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory response</topic><topic>Leeches - chemistry</topic><topic>Lipopolysaccharides - administration & dosage</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lipoproteins, LDL - administration & dosage</topic><topic>Lipoproteins, LDL - toxicity</topic><topic>Liver X Receptors - genetics</topic><topic>Liver X Receptors - metabolism</topic><topic>Macrophages - drug effects</topic><topic>Mice</topic><topic>Peptides - chemistry</topic><topic>Peptides - pharmacology</topic><topic>Polypeptides</topic><topic>RAW 264.7 Cells</topic><topic>Reactive Oxygen Species</topic><topic>Scavenger Receptors, Class E - genetics</topic><topic>Scavenger Receptors, Class E - metabolism</topic><topic>THP-1 Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Jing</creatorcontrib><creatorcontrib>Chen, Xuenan</creatorcontrib><creatorcontrib>Xu, Xiaohao</creatorcontrib><creatorcontrib>Liu, Jianzeng</creatorcontrib><creatorcontrib>Zhang, Zepeng</creatorcontrib><creatorcontrib>Wang, Mingxing</creatorcontrib><creatorcontrib>Li, Xiangzhu</creatorcontrib><creatorcontrib>Chen, Hong</creatorcontrib><creatorcontrib>Zhao, Daqing</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Zhao, Dexi</creatorcontrib><creatorcontrib>Cong, Deyu</creatorcontrib><creatorcontrib>Li, Xiangyan</creatorcontrib><creatorcontrib>Sun, Liwei</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Jing</au><au>Chen, Xuenan</au><au>Xu, Xiaohao</au><au>Liu, Jianzeng</au><au>Zhang, Zepeng</au><au>Wang, Mingxing</au><au>Li, Xiangzhu</au><au>Chen, Hong</au><au>Zhao, Daqing</au><au>Wang, Jian</au><au>Zhao, Dexi</au><au>Cong, Deyu</au><au>Li, Xiangyan</au><au>Sun, Liwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Active polypeptides from Hirudo inhibit endothelial cell inflammation and macrophage foam cell formation by regulating the LOX-1/LXR-α/ABCA1 pathway</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2019-07</date><risdate>2019</risdate><volume>115</volume><spage>108840</spage><epage>108840</epage><pages>108840-108840</pages><artnum>108840</artnum><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>[Display omitted]
•HE (PP) inhibits adhesion and inflammatory response in endothelial cells.•HE (PP) suppresses foam cell formation and apoptosis in macrophages.•HE (PP) inhibits lipid accumulation by regulating LOX-1/LXR-α/ABCA1 pathway.•HE (PP) is identified as a potential novel therapy for atherosclerosis prevention.
Hirudo is an important Chinese medicine that has been widely used in patients with thrombosis-related diseases. We aimed to evaluate the protective effect and potential mechanism of Hirudo extract (HE) on the process of atherosclerosis (AS) as well as identify its active components in the lipopolysaccharide (LPS) - or oxidized low-density lipoprotein (ox-LDL)-induced cell models.
After treatment, adhesion molecules and pro-inflammatory cytokines induced by LPS were examined by qPCR and ELISA. ROS production, cell apoptosis, and lipid accumulation in ox-LDL-induced cells were analyzed by flow cytometry, qPCR, western blotting, and immunofluorescence staining. In addition, the main active components of HE were identified and analyzed for preventing the progression of AS.
In this study, we found that HE pretreatment for 48 h significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Moreover, HE attenuated ox-LDL-induced ROS accumulation and apoptosis in macrophage cells via mitochondrial apoptotic pathways. Additionally, HE pretreatment effectively inhibited cholesterol uptake and increased cholesterol efflux by regulating the LOX-1/LXR-α/ABCA1 pathway. Importantly, the polypeptides from HE (PP) with a molecular weight < 10,000 Da accounted for about 62.9% of the total amount of polypeptides, which in turn may be active components of HE that are responsible for inhibiting inflammation, foam cell formation and apoptosis.
PP from HE potently inhibits endothelial cell inflammatory injury and macrophage foam cell formation and apoptosis by regulating the LOX-1/LXR-α/ABCA1 pathway, thereby providing additional support to the beneficial effects of HE in preventing AS.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>31048189</pmid><doi>10.1016/j.biopha.2019.108840</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals ATP Binding Cassette Transporter 1 - genetics ATP Binding Cassette Transporter 1 - metabolism Cell Adhesion - drug effects Cholesterol - metabolism Cholesterol uptake and efflux Dose-Response Relationship, Drug Foam cell formation Foam Cells - drug effects Gene Expression Regulation - drug effects Hirudo extract Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - metabolism Humans Inflammation - drug therapy Inflammation - metabolism Inflammatory response Leeches - chemistry Lipopolysaccharides - administration & dosage Lipopolysaccharides - toxicity Lipoproteins, LDL - administration & dosage Lipoproteins, LDL - toxicity Liver X Receptors - genetics Liver X Receptors - metabolism Macrophages - drug effects Mice Peptides - chemistry Peptides - pharmacology Polypeptides RAW 264.7 Cells Reactive Oxygen Species Scavenger Receptors, Class E - genetics Scavenger Receptors, Class E - metabolism THP-1 Cells |
| title | Active polypeptides from Hirudo inhibit endothelial cell inflammation and macrophage foam cell formation by regulating the LOX-1/LXR-α/ABCA1 pathway |
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