Atorvastatin inhibits Lipopolysaccharide expression
Purpose This study aimed to explore the differential effects of varying doses of atorvastatin on antagonizing lipopolysaccharide (LPS)-induced endothelial inflammation based on heme oxygenase 1 (HO-1) expression. Method Vascular endothelial inflammatory injury was induced in 40 Sprague-Dawley rats b...
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Veröffentlicht in: | PloS one 2024-08, Vol.19 (8), p.e0308823 |
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description | Purpose This study aimed to explore the differential effects of varying doses of atorvastatin on antagonizing lipopolysaccharide (LPS)-induced endothelial inflammation based on heme oxygenase 1 (HO-1) expression. Method Vascular endothelial inflammatory injury was induced in 40 Sprague-Dawley rats by intraperitoneal injection of LPS. These rats were randomly divided into control, low-dose atorvastatin, high-dose atorvastatin, and HO-1 blocking groups. Seven days after treatment, all rats were sacrificed, and heart-derived peripheral blood was collected to measure the serum concentrations of bilirubin, alanine aminotransferase (ALT), total cholesterol, malondialdehyde, endothelial cell protein C receptor, endothelin-1, von Willebrand factor, and soluble thrombomodulin. Meanwhile, the number of circulating endothelial cells was determined using flow cytometry. Vascular tissues from descending aorta of rats from each group were extracted to detect the expression level of HO-1. Results After different doses of atorvastatin intervention, the above inflammatory indices were decreased, and HO-1 expression and ALT concentration were increased in the atorvastatin-treated group of rats compared with the control group. These changes were more pronounced in the high-dose statin group (P 0.05). Conclusion For LPS-induced vascular inflammation, high-dose atorvastatin exerts potent anti-inflammatory and vascular endothelial protection effects by inducing HO-1 expression. |
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Method Vascular endothelial inflammatory injury was induced in 40 Sprague-Dawley rats by intraperitoneal injection of LPS. These rats were randomly divided into control, low-dose atorvastatin, high-dose atorvastatin, and HO-1 blocking groups. Seven days after treatment, all rats were sacrificed, and heart-derived peripheral blood was collected to measure the serum concentrations of bilirubin, alanine aminotransferase (ALT), total cholesterol, malondialdehyde, endothelial cell protein C receptor, endothelin-1, von Willebrand factor, and soluble thrombomodulin. Meanwhile, the number of circulating endothelial cells was determined using flow cytometry. Vascular tissues from descending aorta of rats from each group were extracted to detect the expression level of HO-1. Results After different doses of atorvastatin intervention, the above inflammatory indices were decreased, and HO-1 expression and ALT concentration were increased in the atorvastatin-treated group of rats compared with the control group. These changes were more pronounced in the high-dose statin group (P 0.05). Conclusion For LPS-induced vascular inflammation, high-dose atorvastatin exerts potent anti-inflammatory and vascular endothelial protection effects by inducing HO-1 expression.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0308823</identifier><language>eng</language><publisher>Public Library of Science</publisher><subject>Antilipemic agents ; Bilirubin ; Endothelin ; Endothelium ; Heme ; Inflammation ; Protein C ; Von Willebrand factor</subject><ispartof>PloS one, 2024-08, Vol.19 (8), p.e0308823</ispartof><rights>COPYRIGHT 2024 Public Library of Science</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids></links><search><creatorcontrib>Luo, Jian</creatorcontrib><creatorcontrib>Zhu, Qian</creatorcontrib><creatorcontrib>Huang, Keming</creatorcontrib><creatorcontrib>Wen, Xue</creatorcontrib><creatorcontrib>Peng, Yongquan</creatorcontrib><creatorcontrib>Chen, Gong</creatorcontrib><creatorcontrib>Wei, Gang</creatorcontrib><title>Atorvastatin inhibits Lipopolysaccharide expression</title><title>PloS one</title><description>Purpose This study aimed to explore the differential effects of varying doses of atorvastatin on antagonizing lipopolysaccharide (LPS)-induced endothelial inflammation based on heme oxygenase 1 (HO-1) expression. Method Vascular endothelial inflammatory injury was induced in 40 Sprague-Dawley rats by intraperitoneal injection of LPS. These rats were randomly divided into control, low-dose atorvastatin, high-dose atorvastatin, and HO-1 blocking groups. Seven days after treatment, all rats were sacrificed, and heart-derived peripheral blood was collected to measure the serum concentrations of bilirubin, alanine aminotransferase (ALT), total cholesterol, malondialdehyde, endothelial cell protein C receptor, endothelin-1, von Willebrand factor, and soluble thrombomodulin. Meanwhile, the number of circulating endothelial cells was determined using flow cytometry. Vascular tissues from descending aorta of rats from each group were extracted to detect the expression level of HO-1. Results After different doses of atorvastatin intervention, the above inflammatory indices were decreased, and HO-1 expression and ALT concentration were increased in the atorvastatin-treated group of rats compared with the control group. These changes were more pronounced in the high-dose statin group (P 0.05). Conclusion For LPS-induced vascular inflammation, high-dose atorvastatin exerts potent anti-inflammatory and vascular endothelial protection effects by inducing HO-1 expression.</description><subject>Antilipemic agents</subject><subject>Bilirubin</subject><subject>Endothelin</subject><subject>Endothelium</subject><subject>Heme</subject><subject>Inflammation</subject><subject>Protein C</subject><subject>Von Willebrand factor</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNptUMFqwzAMNWODdd3-YIfAzslsK3GcYyjrNgjs0ntRFbt1Se0QZ2P7-xq2Qw9DSO_xeHogMfYoeCGgFs_H8Dl5HIoxeFNw4FpLuGIL0YDMleRwfcFv2V2MR84r0EotGLRzmL4wzjg7nzl_cDs3x6xzYxjD8BOR6ICT601mvsfJxOiCv2c3FodoHv5wyTbrl83qLe8-Xt9XbZfvVQ251dhXom-MboRSWFGvpCWSmpCDFKmt5JUELXRTm9KoXZUGJwJJttQES_b0G7vHwWydt2GekE4u0rbVvGzSAQDJVfzjStWbk6P0EOuSfrFwBpgeWYY</recordid><startdate>20240815</startdate><enddate>20240815</enddate><creator>Luo, Jian</creator><creator>Zhu, Qian</creator><creator>Huang, Keming</creator><creator>Wen, Xue</creator><creator>Peng, Yongquan</creator><creator>Chen, Gong</creator><creator>Wei, Gang</creator><general>Public Library of Science</general><scope/></search><sort><creationdate>20240815</creationdate><title>Atorvastatin inhibits Lipopolysaccharide expression</title><author>Luo, Jian ; Zhu, Qian ; Huang, Keming ; Wen, Xue ; Peng, Yongquan ; Chen, Gong ; Wei, Gang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g673-f8ad51d9e89166a5cd62fcc28ca0321032f2052381897e4e6b54e60cc32cf48c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antilipemic agents</topic><topic>Bilirubin</topic><topic>Endothelin</topic><topic>Endothelium</topic><topic>Heme</topic><topic>Inflammation</topic><topic>Protein C</topic><topic>Von Willebrand factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Jian</creatorcontrib><creatorcontrib>Zhu, Qian</creatorcontrib><creatorcontrib>Huang, Keming</creatorcontrib><creatorcontrib>Wen, Xue</creatorcontrib><creatorcontrib>Peng, Yongquan</creatorcontrib><creatorcontrib>Chen, Gong</creatorcontrib><creatorcontrib>Wei, Gang</creatorcontrib><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Jian</au><au>Zhu, Qian</au><au>Huang, Keming</au><au>Wen, Xue</au><au>Peng, Yongquan</au><au>Chen, Gong</au><au>Wei, Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atorvastatin inhibits Lipopolysaccharide expression</atitle><jtitle>PloS one</jtitle><date>2024-08-15</date><risdate>2024</risdate><volume>19</volume><issue>8</issue><spage>e0308823</spage><pages>e0308823-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Purpose This study aimed to explore the differential effects of varying doses of atorvastatin on antagonizing lipopolysaccharide (LPS)-induced endothelial inflammation based on heme oxygenase 1 (HO-1) expression. Method Vascular endothelial inflammatory injury was induced in 40 Sprague-Dawley rats by intraperitoneal injection of LPS. These rats were randomly divided into control, low-dose atorvastatin, high-dose atorvastatin, and HO-1 blocking groups. Seven days after treatment, all rats were sacrificed, and heart-derived peripheral blood was collected to measure the serum concentrations of bilirubin, alanine aminotransferase (ALT), total cholesterol, malondialdehyde, endothelial cell protein C receptor, endothelin-1, von Willebrand factor, and soluble thrombomodulin. Meanwhile, the number of circulating endothelial cells was determined using flow cytometry. Vascular tissues from descending aorta of rats from each group were extracted to detect the expression level of HO-1. Results After different doses of atorvastatin intervention, the above inflammatory indices were decreased, and HO-1 expression and ALT concentration were increased in the atorvastatin-treated group of rats compared with the control group. These changes were more pronounced in the high-dose statin group (P 0.05). Conclusion For LPS-induced vascular inflammation, high-dose atorvastatin exerts potent anti-inflammatory and vascular endothelial protection effects by inducing HO-1 expression.</abstract><pub>Public Library of Science</pub><doi>10.1371/journal.pone.0308823</doi></addata></record> |
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source | DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
subjects | Antilipemic agents Bilirubin Endothelin Endothelium Heme Inflammation Protein C Von Willebrand factor |
title | Atorvastatin inhibits Lipopolysaccharide expression |
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