Boswellic acid inhibits inflammatory angiogenesis in a murine sponge model
The aim of the present study was to investigate the effects of boswellic acid (BA) on key components of inflammatory angiogenesis in the murine cannulated sponge implant angiogenesis model. Polyester–polyurethane sponges, used as a framework for fibrovascular tissue growth, were implanted in Swiss a...
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Veröffentlicht in: | Microvascular research 2011-11, Vol.82 (3), p.263-268 |
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description | The aim of the present study was to investigate the effects of boswellic acid (BA) on key components of inflammatory angiogenesis in the murine cannulated sponge implant angiogenesis model. Polyester–polyurethane sponges, used as a framework for fibrovascular tissue growth, were implanted in Swiss albino mice and BA (12.5 or 25mg/kg/day) was given through installed cannulas for nine days. The implants collected at day 9 post-implantation were processed for the assessment of hemoglobin (Hb). Relevant levels of inflammatory, angiogenic and fibrogenic cytokines were also determined. BA treatment resulted in significant decrease in sponge vascularization (Hb content) and in vascular endothelial growth factor (VEGF) and transforming growth factor (TGF-β1) at both doses. Further, BA decreased expression of VEGF and CD31 and reduced % microvessel density (MVD) in sponge implants. A regulatory function of BA on multiple parameters of the main components of inflammatory angiogenesis has been revealed giving an insight into the potential therapeutic use underlying the actions of BA.
► BA inhibits sponge vascularization in sponge implant angiogenesis model. ► It downregulates VEGF, TNF-α and TGF-β expression. ► It reduced CD31 expression and decreased % microvessel density (MVD). |
doi_str_mv | 10.1016/j.mvr.2011.08.002 |
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► BA inhibits sponge vascularization in sponge implant angiogenesis model. ► It downregulates VEGF, TNF-α and TGF-β expression. ► It reduced CD31 expression and decreased % microvessel density (MVD).</description><identifier>ISSN: 0026-2862</identifier><identifier>EISSN: 1095-9319</identifier><identifier>DOI: 10.1016/j.mvr.2011.08.002</identifier><identifier>PMID: 21864545</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiogenesis Inhibitors - pharmacology ; Animals ; Anti-Inflammatory Agents - pharmacology ; Capillaries - drug effects ; Capillaries - metabolism ; Capillaries - pathology ; Capillaries - physiopathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Hemoglobins - metabolism ; Inflammation - etiology ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - physiopathology ; Inflammation - prevention & control ; Inflammation Mediators - metabolism ; Male ; Mice ; Neovascularization, Pathologic - etiology ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - pathology ; Neovascularization, Pathologic - physiopathology ; Neovascularization, Pathologic - prevention & control ; Neovascularization, Physiologic - drug effects ; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism ; Polyurethanes ; Surgical Sponges ; Time Factors ; Transforming Growth Factor beta1 - metabolism ; Triterpenes - pharmacology ; Tumor Necrosis Factor-alpha - metabolism ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Microvascular research, 2011-11, Vol.82 (3), p.263-268</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-b526b7e89d94305c511c2e9ae9b06504a8bf511df4324baa53b31ad6eb43f4e73</citedby><cites>FETCH-LOGICAL-c418t-b526b7e89d94305c511c2e9ae9b06504a8bf511df4324baa53b31ad6eb43f4e73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0026286211001476$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21864545$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saraswati, Sarita</creatorcontrib><creatorcontrib>Pandey, Maneesha</creatorcontrib><creatorcontrib>Mathur, Rajani</creatorcontrib><creatorcontrib>Agrawal, S.S.</creatorcontrib><title>Boswellic acid inhibits inflammatory angiogenesis in a murine sponge model</title><title>Microvascular research</title><addtitle>Microvasc Res</addtitle><description>The aim of the present study was to investigate the effects of boswellic acid (BA) on key components of inflammatory angiogenesis in the murine cannulated sponge implant angiogenesis model. Polyester–polyurethane sponges, used as a framework for fibrovascular tissue growth, were implanted in Swiss albino mice and BA (12.5 or 25mg/kg/day) was given through installed cannulas for nine days. The implants collected at day 9 post-implantation were processed for the assessment of hemoglobin (Hb). Relevant levels of inflammatory, angiogenic and fibrogenic cytokines were also determined. BA treatment resulted in significant decrease in sponge vascularization (Hb content) and in vascular endothelial growth factor (VEGF) and transforming growth factor (TGF-β1) at both doses. Further, BA decreased expression of VEGF and CD31 and reduced % microvessel density (MVD) in sponge implants. A regulatory function of BA on multiple parameters of the main components of inflammatory angiogenesis has been revealed giving an insight into the potential therapeutic use underlying the actions of BA.
► BA inhibits sponge vascularization in sponge implant angiogenesis model. ► It downregulates VEGF, TNF-α and TGF-β expression. ► It reduced CD31 expression and decreased % microvessel density (MVD).</description><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Capillaries - drug effects</subject><subject>Capillaries - metabolism</subject><subject>Capillaries - pathology</subject><subject>Capillaries - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Hemoglobins - metabolism</subject><subject>Inflammation - etiology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation - physiopathology</subject><subject>Inflammation - prevention & control</subject><subject>Inflammation Mediators - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Neovascularization, Pathologic - etiology</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Neovascularization, Pathologic - physiopathology</subject><subject>Neovascularization, Pathologic - prevention & control</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</subject><subject>Polyurethanes</subject><subject>Surgical Sponges</subject><subject>Time Factors</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Triterpenes - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>0026-2862</issn><issn>1095-9319</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kD1PwzAQhi0EoqXwA1hQNqYE27HTWExQ8alKLDBb_rgUV0lc7LSo_x5XLYxMd7p77pXuQeiS4IJgUt0si24TCooJKXBdYEyP0JhgwXNREnGMxmlS5bSu6AidxbjECeSCnqIRJXXFOONj9Hrv4ze0rTOZMs5mrv902g0xNU2ruk4NPmwz1S-cX0AP0e02mcq6dXA9ZHHl-wVknbfQnqOTRrURLg51gj4eH95nz_n87elldjfPDSP1kGtOKz2FWljBSswNJ8RQEAqExhXHTNW6STPbsJIyrRQvdUmUrUCzsmEwLSfoep-7Cv5rDXGQnYsm_aB68OsoBWaY4CkliSR70gQfY4BGroLrVNhKguXOoFzKZFDuDEpcy-Qr3Vwd0te6A_t38assAbd7ANKPGwdBRuOgN2BdADNI690_8T9WrYGc</recordid><startdate>201111</startdate><enddate>201111</enddate><creator>Saraswati, Sarita</creator><creator>Pandey, Maneesha</creator><creator>Mathur, Rajani</creator><creator>Agrawal, S.S.</creator><general>Elsevier Inc</general><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>201111</creationdate><title>Boswellic acid inhibits inflammatory angiogenesis in a murine sponge model</title><author>Saraswati, Sarita ; Pandey, Maneesha ; Mathur, Rajani ; Agrawal, S.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-b526b7e89d94305c511c2e9ae9b06504a8bf511df4324baa53b31ad6eb43f4e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Angiogenesis Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Capillaries - drug effects</topic><topic>Capillaries - metabolism</topic><topic>Capillaries - pathology</topic><topic>Capillaries - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Hemoglobins - metabolism</topic><topic>Inflammation - etiology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation - physiopathology</topic><topic>Inflammation - prevention & control</topic><topic>Inflammation Mediators - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Neovascularization, Pathologic - etiology</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Neovascularization, Pathologic - physiopathology</topic><topic>Neovascularization, Pathologic - prevention & control</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</topic><topic>Polyurethanes</topic><topic>Surgical Sponges</topic><topic>Time Factors</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Triterpenes - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saraswati, Sarita</creatorcontrib><creatorcontrib>Pandey, Maneesha</creatorcontrib><creatorcontrib>Mathur, Rajani</creatorcontrib><creatorcontrib>Agrawal, S.S.</creatorcontrib><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>Microvascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saraswati, Sarita</au><au>Pandey, Maneesha</au><au>Mathur, Rajani</au><au>Agrawal, S.S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Boswellic acid inhibits inflammatory angiogenesis in a murine sponge model</atitle><jtitle>Microvascular research</jtitle><addtitle>Microvasc Res</addtitle><date>2011-11</date><risdate>2011</risdate><volume>82</volume><issue>3</issue><spage>263</spage><epage>268</epage><pages>263-268</pages><issn>0026-2862</issn><eissn>1095-9319</eissn><abstract>The aim of the present study was to investigate the effects of boswellic acid (BA) on key components of inflammatory angiogenesis in the murine cannulated sponge implant angiogenesis model. Polyester–polyurethane sponges, used as a framework for fibrovascular tissue growth, were implanted in Swiss albino mice and BA (12.5 or 25mg/kg/day) was given through installed cannulas for nine days. The implants collected at day 9 post-implantation were processed for the assessment of hemoglobin (Hb). Relevant levels of inflammatory, angiogenic and fibrogenic cytokines were also determined. BA treatment resulted in significant decrease in sponge vascularization (Hb content) and in vascular endothelial growth factor (VEGF) and transforming growth factor (TGF-β1) at both doses. Further, BA decreased expression of VEGF and CD31 and reduced % microvessel density (MVD) in sponge implants. A regulatory function of BA on multiple parameters of the main components of inflammatory angiogenesis has been revealed giving an insight into the potential therapeutic use underlying the actions of BA.
► BA inhibits sponge vascularization in sponge implant angiogenesis model. ► It downregulates VEGF, TNF-α and TGF-β expression. ► It reduced CD31 expression and decreased % microvessel density (MVD).</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>21864545</pmid><doi>10.1016/j.mvr.2011.08.002</doi><tpages>6</tpages></addata></record> |
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subjects | Angiogenesis Inhibitors - pharmacology Animals Anti-Inflammatory Agents - pharmacology Capillaries - drug effects Capillaries - metabolism Capillaries - pathology Capillaries - physiopathology Disease Models, Animal Dose-Response Relationship, Drug Hemoglobins - metabolism Inflammation - etiology Inflammation - metabolism Inflammation - pathology Inflammation - physiopathology Inflammation - prevention & control Inflammation Mediators - metabolism Male Mice Neovascularization, Pathologic - etiology Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology Neovascularization, Pathologic - physiopathology Neovascularization, Pathologic - prevention & control Neovascularization, Physiologic - drug effects Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Polyurethanes Surgical Sponges Time Factors Transforming Growth Factor beta1 - metabolism Triterpenes - pharmacology Tumor Necrosis Factor-alpha - metabolism Vascular Endothelial Growth Factor A - metabolism |
title | Boswellic acid inhibits inflammatory angiogenesis in a murine sponge model |
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