The cyclic adenosine monophosphate elevating medicine, forskolin, reduces neointimal formation and atherogenesis in mice
Rattachement africain : cn. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Neointimal formation and atherogenesis are major vascular complications following percutaneous coronary intervention, and there is lack of pharmacological therapy. This study was aimed to examine the effect of forskolin (FSK), a cyclic adenosine monophosphate (cAMP)-elevating agent, on vascular response to angioplasty wire injury and on atherogenesis in mice. Forskolin treatment reduced neointima formation at 7 and 28 days after wire injury. Early morphometrics of the injured vessels revealed that FSK treatment enhanced endothelial repair and reduced inflammatory cell infiltration. In vitro treatment of primary aortic cells with FSK, at 3-100 μmol/L, increased endothelial cell proliferation, whereas FSK, at 30-100 μmol/L, inhibited smooth muscle cell proliferation. FSK inhibited lipopolysaccharide-induced leucocyte-endothelial interaction in vitro and in vivo. In a mouse model of atherosclerosis driven by dyslipidaemia and hypertension, FSK administration increased endothelial repair and reduced atherosclerotic plaque formation, without affecting blood pressure, plasma lipids or aortic aneurysms formation. In summary, FSK, at doses relevant to human therapeutic use, protects against neointimal hyperplasia and atherogenesis, and this is attributable to its activities on pro-endothelial repair and anti-inflammation. This study raises a potential of clinical use of FSK as an adjunct therapy to prevent restenosis and atherosclerosis after percutaneous coronary intervention.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- The cyclic adenosine monophosphate elevating medicine, forskolin, reduces neointimal formation and atherogenesis in mice
- Date Crossref
- 18/08/2020
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
-
Chinese Academy of Medical Sciences & Peking Union Medical College pays non établi dans la noticeUniversité ou école supérieure
-
Peking University Department of Integration of Chinese and Western Medicine Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education pays non établi dans la noticeUniversité ou école supérieure
-
Peking University Cancer Hospital pays non établi dans la noticeÉtablissement de santé
-
State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China State Key Laboratory of Cardiovascular Disease pays non établi dans la noticeUniversité ou école supérieure
-
Clinical Pharmacology Center National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China pays non établi dans la noticeUniversité ou école supérieure
Chinese Academy of Medical Sciences & Peking Union Medical College, Department of Integration of Chinese and Western Medicine Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education — Peking University et Peking University Cancer Hospital, avec 2 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.