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Magnolol inhibits venous remodeling in mice
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Veröffentlicht in: | Scientific reports 7(2017) Artikel-Nummer 17820, 13 Seiten |
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Personen und Körperschaften: | , , , |
Titel: | Magnolol inhibits venous remodeling in mice/ Hanna Kuk, Caroline Arnold, Ralph Meyer, Markus Hecker & Thomas Korff |
Format: | E-Book-Kapitel |
Sprache: | Englisch |
veröffentlicht: |
19 December 2017
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Gesamtaufnahme: |
: Scientific reports, 7(2017) Artikel-Nummer 17820, 13 Seiten
, volume:7 |
Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
Zusammenfassung: | Due to gravity the venous vasculature in the lower extremities is exposed to elevated pressure levels which may be amplified by obesity or pregnancy. As a consequence, venules dilate and may be slowly transformed into varicose or spider veins. In fact, chronically elevated venous pressure was sufficient to cause the corkscrew-like enlargement of superficial veins in mice. We hypothesized that biomechanical activation of endothelial cells contributes to this process and investigated the inhibitory capacity of Magnolol in this context - a natural compound that features multiple properties counteracting cellular stress. While Magnolol did not influence endothelial capillary sprout formation, it interfered with proliferation, ERK1/2 activity, gelatinase activity as well as baseline production of reactive oxygen species in these cells or murine veins. The anti-oxidative and anti-proliferative capacity of Magnolol was mediated through stimulation of heme oxygenase-1 expression. Finally, local transdermal application of Magnolol attenuated pressure-mediated development of varicose/spider veins in mice and was accompanied by the absence of proliferating and MMP-2 positive endothelial cells. Collectively, our data identified Magnolol as a potent inhibitor of biomechanically evoked endothelial cell activity during pressure-mediated venous remodeling processes which contribute to the development of varicose and spider veins. |
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Beschreibung: | Gesehen am 12.04.2018 |
Umfang: | 13 |
ISSN: |
2045-2322
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DOI: | 10.1038/s41598-017-17910-0 |