Acta pharmacologica Sinica, 2017-10, Vol.38 (10), p.1329-1339
2017
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- Autor(en) / Beteiligte
- Titel
- Curcumin enhances vascular contractility via induction of myocardin in mouse smooth muscle cells
- Ist Teil von
- Acta pharmacologica Sinica, 2017-10, Vol.38 (10), p.1329-1339
- Ort / Verlag
- United States: Nature Publishing Group
- Erscheinungsjahr
- 2017
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- A variety of cardiovascular diseases is accompanied by the loss of vascular contractility. This study sought to investigate the effects of curcumin, a natural polyphenolic compound present in turmeric, on mouse vascular contractility and the underlying mechanisms. After mice were administered curcumin （100 mg kg-1-d-1, ig） for 6 weeks, thecontractile responses of the thoracic aorta to KCI and phenylephrine were significantly enhanced compared with the control group. Furthermore, the contractility of vascular smooth muscle （SM） was significantly enhanced after incubation in curcumin （25 μmol/L） for 4 d, which was accompanied by upregulated expression of SM marker contractile proteins SM22a and SM a-actin, in cultured vascular smooth muscle cells （VSMCs）, curcumin （10, 25, 50 μmol/L） significantly increased the expression of myocardin, a ＂master regulator＂ of SM gene expression. Curcumin treatment also significantly increased the levels of caveolin-1 in VSMCs. We found that as a result of the upregulation of caveolin-1, curcumin blocked the activation of Notch1 and thereby abolished Notchl-inhibited myocardin expression. Knockdown of caveolin-1 or activation of Notch1 signaling with Jaggedl （2 pg/mL） diminished these effects of curcumin in VSMCs. These findings suggest that curcumin induces the expression of myocardin in mouse smooth muscle cells via a variety of mechanisms, including caveolin-l-mediated inhibition of Notch1 activation and Notchl-mediated repression of myocardin expression. This may represent a novel pathway, through which curcumin protects blood vessels via the beneficial regulation of SM contractility.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1671-4083eISSN: 1745-7254DOI: 10.1038/aps.2017.18Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5630668
- Format
- –
- Schlagworte
- Actin, Actins - metabolism, Activation, Animals, Anti-Inflammatory Agents, Non-Steroidal - administration & dosage, Anti-Inflammatory Agents, Non-Steroidal - pharmacology, Aorta, Aorta, Thoracic - drug effects, Aorta, Thoracic - metabolism, Blood vessels, Cardiovascular diseases, Caveolin, Caveolin 1 - genetics, Caveolin 1 - metabolism, Caveolin-1, Cells, Cultured, Contractility, Curcumin, Curcumin - administration & dosage, Curcumin - pharmacology, Dose-Response Relationship, Drug, Gene expression, Gene Knockdown Techniques, Humans, Immunoglobulins, Jagged1 protein, Male, Mice, Mice, Inbred C57BL, Muscle contraction, Muscle Contraction - drug effects, Muscle, Smooth, Vascular - cytology, Muscle, Smooth, Vascular - drug effects, Myocytes, Smooth Muscle - drug effects, Myocytes, Smooth Muscle - metabolism, Notch1 protein, Nuclear Proteins - genetics, Original, Phenylephrine, Potassium chloride, Proteins, Receptor, Notch1 - metabolism, Rodents, Signal Transduction - drug effects, Smooth muscle, Thorax, Trans-Activators - genetics, Up-Regulation - drug effects, VSMC, 功能增强, 多酚类化合物, 姜黄素, 小鼠, 血管平滑肌细胞, 血管收缩, 诱导