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.

中文翻译：

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环状腺苷一磷酸增强药物福司可林减少小鼠新内膜的形成和动脉粥样硬化的形成。

新内膜形成和动脉粥样硬化是经皮冠状动脉介入治疗后的主要血管并发症，并且缺乏药物治疗。这项研究的目的是研究环式单磷酸腺苷（cAMP）升高剂福斯高林（FSK）对血管对血管成形术导线损伤的反应以及对小鼠动脉粥样硬化的影响。在钢丝损伤后的7天和28天，福斯克林治疗减少了新内膜的形成。受伤血管的早期形态计量学表明，FSK治疗可增强内皮修复并减少炎症细胞浸润。以3-100μmol/ L的FSK体外处理主动脉主动脉细胞可增加内皮细胞增殖，而以30-100μmol/ L的FSK则可抑制平滑肌细胞增殖。FSK在体内外均抑制脂多糖诱导的白细胞-内皮相互作用。在血脂异常和高血压驱动的小鼠动脉粥样硬化模型中，FSK给药可增加内皮修复和减少动脉粥样硬化斑块形成，而不会影响血压，血浆脂质或主动脉瘤的形成。总之，与人类治疗用途相关的剂量的FSK可预防新内膜增生和动脉粥样硬化的形成，这归因于其对内皮前修复和抗炎的作用。这项研究提高了FSK作为预防经皮冠状动脉介入治疗后再狭窄和动脉粥样硬化的辅助疗法的临床应用潜力。FSK给药可增加内皮修复和减少动脉粥样硬化斑块的形成，而不会影响血压，血浆脂质或主动脉瘤的形成。总之，与人类治疗用途相关的剂量的FSK可预防新内膜增生和动脉粥样硬化的形成，这归因于其对内皮前修复和抗炎的作用。这项研究提高了FSK作为预防经皮冠状动脉介入治疗后再狭窄和动脉粥样硬化的辅助疗法的临床应用潜力。FSK给药可增加内皮修复和减少动脉粥样硬化斑块的形成，而不会影响血压，血浆脂质或主动脉瘤的形成。总之，与人类治疗用途相关的剂量的FSK可预防新内膜增生和动脉粥样硬化的形成，这归因于其对内皮前修复和抗炎的作用。这项研究提高了FSK作为预防经皮冠状动脉介入治疗后再狭窄和动脉粥样硬化的辅助疗法的临床应用潜力。这归因于其在内皮前修复和抗炎方面的活动。这项研究提高了FSK作为预防经皮冠状动脉介入治疗后再狭窄和动脉粥样硬化的辅助疗法的临床应用潜力。这归因于其在内皮前修复和抗炎方面的活动。这项研究提高了FSK作为预防经皮冠状动脉介入治疗后再狭窄和动脉粥样硬化的辅助疗法的临床应用潜力。