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Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway
Background Atherosclerosis is a chronic inflammatory disease of arterial wall, which is closely related to inflammatory reaction. In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway. Methods (1) ApoE.sup.-/- mice were fed with high-fat diet to est...
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Published in: | BMC complementary medicine and therapies 2023-03, Vol.23 (1) |
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description | Background Atherosclerosis is a chronic inflammatory disease of arterial wall, which is closely related to inflammatory reaction. In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway. Methods (1) ApoE.sup.-/- mice were fed with high-fat diet to establish atherosclerotic model, while C57 with the same genetic background was fed with common diet as control group. Body weight was recorded and blood lipids were detected. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and plaque formation was detected by HE and oil red O staining. (2) Lipopolysaccharide interfered with Human Umbilical Vein Endothelial Cells (HUVECs) and RAW264.7 to form inflammatory model, and was treated with isorhynchophylline. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and the ability of cell migration was detected by Transwell and scratch test. Results (1) the expression of NLRP3, NF- κB, IL-18 and Caspase-1 in aorta of model group was higher than that of control group, and plaque formation was obvious. (2) the expressions of NLRP3, NF- κB, IL-18 and Caspase-1 in HUVECs and RAW264.7 model groups were higher than those in control group, while isorhynchophylline decreased their expression and enhanced cell migration ability. Conclusion Isorhynchophylline can reduce the inflammatory reaction induced by lipopolysaccharide and promote the ability of cell migration. Keywords: Inflammation, NF-κB, NLRP3, Human umbilical vein endothelial cells, Isorhynchophylline |
doi_str_mv | 10.1186/s12906-023-03902-3 |
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In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway. Methods (1) ApoE.sup.-/- mice were fed with high-fat diet to establish atherosclerotic model, while C57 with the same genetic background was fed with common diet as control group. Body weight was recorded and blood lipids were detected. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and plaque formation was detected by HE and oil red O staining. (2) Lipopolysaccharide interfered with Human Umbilical Vein Endothelial Cells (HUVECs) and RAW264.7 to form inflammatory model, and was treated with isorhynchophylline. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and the ability of cell migration was detected by Transwell and scratch test. Results (1) the expression of NLRP3, NF- κB, IL-18 and Caspase-1 in aorta of model group was higher than that of control group, and plaque formation was obvious. (2) the expressions of NLRP3, NF- κB, IL-18 and Caspase-1 in HUVECs and RAW264.7 model groups were higher than those in control group, while isorhynchophylline decreased their expression and enhanced cell migration ability. Conclusion Isorhynchophylline can reduce the inflammatory reaction induced by lipopolysaccharide and promote the ability of cell migration. Keywords: Inflammation, NF-κB, NLRP3, Human umbilical vein endothelial cells, Isorhynchophylline</description><identifier>ISSN: 2662-7671</identifier><identifier>EISSN: 2662-7671</identifier><identifier>DOI: 10.1186/s12906-023-03902-3</identifier><language>eng</language><publisher>BioMed Central Ltd</publisher><subject>Analysis ; Blood lipids ; Endothelium ; Inflammation ; Macrophages</subject><ispartof>BMC complementary medicine and therapies, 2023-03, Vol.23 (1)</ispartof><rights>COPYRIGHT 2023 BioMed Central Ltd.</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>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Wang, Li-Hua</creatorcontrib><creatorcontrib>Gu, Zheng-Wei</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Yang, Wen-Qing</creatorcontrib><creatorcontrib>Li, Yun-Lun</creatorcontrib><creatorcontrib>Qi, Dong-Mei</creatorcontrib><creatorcontrib>Wang, Dan-Yang</creatorcontrib><creatorcontrib>Jiang, Hai-Qiang</creatorcontrib><title>Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway</title><title>BMC complementary medicine and therapies</title><description>Background Atherosclerosis is a chronic inflammatory disease of arterial wall, which is closely related to inflammatory reaction. In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway. Methods (1) ApoE.sup.-/- mice were fed with high-fat diet to establish atherosclerotic model, while C57 with the same genetic background was fed with common diet as control group. Body weight was recorded and blood lipids were detected. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and plaque formation was detected by HE and oil red O staining. (2) Lipopolysaccharide interfered with Human Umbilical Vein Endothelial Cells (HUVECs) and RAW264.7 to form inflammatory model, and was treated with isorhynchophylline. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and the ability of cell migration was detected by Transwell and scratch test. Results (1) the expression of NLRP3, NF- κB, IL-18 and Caspase-1 in aorta of model group was higher than that of control group, and plaque formation was obvious. (2) the expressions of NLRP3, NF- κB, IL-18 and Caspase-1 in HUVECs and RAW264.7 model groups were higher than those in control group, while isorhynchophylline decreased their expression and enhanced cell migration ability. Conclusion Isorhynchophylline can reduce the inflammatory reaction induced by lipopolysaccharide and promote the ability of cell migration. Keywords: Inflammation, NF-κB, NLRP3, Human umbilical vein endothelial cells, Isorhynchophylline</description><subject>Analysis</subject><subject>Blood lipids</subject><subject>Endothelium</subject><subject>Inflammation</subject><subject>Macrophages</subject><issn>2662-7671</issn><issn>2662-7671</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNptkM9KAzEQxhdRsNS-gKeA4C1t_uwmu8darBZKFem9TLPZTSS7KZst0rtnH8ijvpgRPVSQOczH8Pu-YSZJLikZU5qLSaCsIAITxjHhBWGYnyQDJgTDUkh6eqTPk1EIz4RElHLJs0Hyugi-M4dWGb8zB-dsq5Ftjd3aPkRROWga6H13QJ0OO98G_T1Gui19b7Sz4JDSzgUEbYkaUF2MgTpCven8vjaxa7Sa48-3j_ebyWr59MhRsHULcVONdtCbFzhcJGcVuKBHv32YrOe369k9Xj7cLWbTJa6LnOFKiVRuhSYlK0VWqqgoJypnGSsLKTURlZS0yFKa8jyDLSgNkKkiV4IrLhUfJlc_sTU4vYnH-b4D1digNlOZkjzNecEiNf6HilXqxirf6srG-R_D9ZHBaHC9Cd7texvfdQx-Afk8g40</recordid><startdate>20230311</startdate><enddate>20230311</enddate><creator>Wang, Li-Hua</creator><creator>Gu, Zheng-Wei</creator><creator>Li, Jie</creator><creator>Yang, Wen-Qing</creator><creator>Li, Yun-Lun</creator><creator>Qi, Dong-Mei</creator><creator>Wang, Dan-Yang</creator><creator>Jiang, Hai-Qiang</creator><general>BioMed Central Ltd</general><scope/></search><sort><creationdate>20230311</creationdate><title>Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway</title><author>Wang, Li-Hua ; Gu, Zheng-Wei ; Li, Jie ; Yang, Wen-Qing ; Li, Yun-Lun ; Qi, Dong-Mei ; Wang, Dan-Yang ; Jiang, Hai-Qiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g982-fc647b6e0d2d65dc6e0130c8252d977e06f77195414385abaceaa5c98c63c37c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Analysis</topic><topic>Blood lipids</topic><topic>Endothelium</topic><topic>Inflammation</topic><topic>Macrophages</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Li-Hua</creatorcontrib><creatorcontrib>Gu, Zheng-Wei</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Yang, Wen-Qing</creatorcontrib><creatorcontrib>Li, Yun-Lun</creatorcontrib><creatorcontrib>Qi, Dong-Mei</creatorcontrib><creatorcontrib>Wang, Dan-Yang</creatorcontrib><creatorcontrib>Jiang, Hai-Qiang</creatorcontrib><jtitle>BMC complementary medicine and therapies</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Li-Hua</au><au>Gu, Zheng-Wei</au><au>Li, Jie</au><au>Yang, Wen-Qing</au><au>Li, Yun-Lun</au><au>Qi, Dong-Mei</au><au>Wang, Dan-Yang</au><au>Jiang, Hai-Qiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway</atitle><jtitle>BMC complementary medicine and therapies</jtitle><date>2023-03-11</date><risdate>2023</risdate><volume>23</volume><issue>1</issue><issn>2662-7671</issn><eissn>2662-7671</eissn><abstract>Background Atherosclerosis is a chronic inflammatory disease of arterial wall, which is closely related to inflammatory reaction. In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway. Methods (1) ApoE.sup.-/- mice were fed with high-fat diet to establish atherosclerotic model, while C57 with the same genetic background was fed with common diet as control group. Body weight was recorded and blood lipids were detected. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and plaque formation was detected by HE and oil red O staining. (2) Lipopolysaccharide interfered with Human Umbilical Vein Endothelial Cells (HUVECs) and RAW264.7 to form inflammatory model, and was treated with isorhynchophylline. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and the ability of cell migration was detected by Transwell and scratch test. Results (1) the expression of NLRP3, NF- κB, IL-18 and Caspase-1 in aorta of model group was higher than that of control group, and plaque formation was obvious. (2) the expressions of NLRP3, NF- κB, IL-18 and Caspase-1 in HUVECs and RAW264.7 model groups were higher than those in control group, while isorhynchophylline decreased their expression and enhanced cell migration ability. Conclusion Isorhynchophylline can reduce the inflammatory reaction induced by lipopolysaccharide and promote the ability of cell migration. Keywords: Inflammation, NF-κB, NLRP3, Human umbilical vein endothelial cells, Isorhynchophylline</abstract><pub>BioMed Central Ltd</pub><doi>10.1186/s12906-023-03902-3</doi></addata></record> |
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title | Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway |
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