The cyclic adenosine monophosphate elevating medicine, forskolin, reduces neointimal formation and atherogenesis in mice
| العنوان: | The cyclic adenosine monophosphate elevating medicine, forskolin, reduces neointimal formation and atherogenesis in mice |
|---|---|
| المؤلفون: | Zekun Peng, Zhenyu Xu, Miao Wang, Yuze Zhang, Xiaoyan Ma, Chuansheng Xu, Liyuan Zhu, Huifeng Hao, Hong Chen, Qiaoling Li |
| المصدر: | Journal of Cellular and Molecular Medicine |
| بيانات النشر: | John Wiley and Sons Inc., 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | 0301 basic medicine, Neointima, Endothelium, endothelium, Myocytes, Smooth Muscle, Inflammation, Blood Pressure, Pharmacology, Muscle, Smooth, Vascular, forskolin, 03 medical and health sciences, chemistry.chemical_compound, restenosis, Mice, 0302 clinical medicine, Restenosis, cAMP, medicine, Cyclic AMP, Leukocytes, Animals, Cyclic adenosine monophosphate, Aorta, Cell Proliferation, Neointimal hyperplasia, Forskolin, Hyperplasia, business.industry, Colforsin, Endothelial Cells, Cell Biology, Original Articles, medicine.disease, Atherosclerosis, Endothelial stem cell, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, medicine.anatomical_structure, chemistry, 030220 oncology & carcinogenesis, Molecular Medicine, Medicine, Original Article, medicine.symptom, business, Signal Transduction |
| الوصف: | 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. |
| اللغة: | English |
| تدمد: | 1582-4934 1582-1838 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bbd1e5e51652443b5beb6edd57b38167Test http://europepmc.org/articles/PMC7520276Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....bbd1e5e51652443b5beb6edd57b38167 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15824934 15821838 |
|---|