title: Boswellic acid inhibits inflammatory angiogenesis in a murine sponge model.
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.
authors.affiliation: Genome Research Laboratory, Delhi Institute of Pharmaceutical Sciences and Research, Pushp Vihar Sec-3, M B Road, New Delhi-110017, India. saritasaraswati@gmail.com
authors.forename: Sarita
authors.initials: S
authors.lastname: Saraswati
authors.forename: Maneesha
authors.initials: M
authors.lastname: Pandey
authors.forename: Rajani
authors.initials: R
authors.lastname: Mathur
authors.forename: S S
authors.initials: SS
authors.lastname: Agrawal
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002196:Capillaries / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D006454:Hemoglobins / Q000378:metabolism; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D051379:Mice; D009389:Neovascularization, Pathologic / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D011140:Polyurethanes; D015503:Surgical Sponges; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014315:Triterpenes / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D000893:Anti-Inflammatory Agents; D006454:Hemoglobins; D018836:Inflammation Mediators; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011140:Polyurethanes; C508961:Tgfb1 protein, mouse; D053773:Transforming Growth Factor beta1; D014315:Triterpenes; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; C054625:boswellic acid