背景和目的：Statin 已知可有效抑制血管平滑肌肥大。Myocardin 為一於血管平滑肌肥厚時增加表現之心臟調控基因。然而，現今對於頸動脈受傷模式下造成血管平滑肌肥厚時，statin 對myocardin 基因表現之影響所知仍有限。方法：為了瞭解statin 對myocardin表現及血管平滑肌肥厚之影響，成年之Sprague-Dawley 鼠頸動脈於氣球導致受傷2 周後造成血管平滑肌肥厚。 Atorvastatin（30 毫克/ 公斤）之後每天投與或以myocardin 之short interfering RNA（siRNA）使用嘗試抑制myocardin 表現及頸動脈受傷模式下造成血管平滑肌肥厚。結果：Myocardin 蛋白及mRNA 表現於頸動脈受傷模式下均上昇。而以atorvastatin 或myocardin siRNA 皆有效減少myocardin 蛋白或myocardin mRNA 之表現。同時進一步回復因頸動脈受傷模式下造成血管平滑肌內膜增厚及血管腔室窄小。免疫組織化學標記亦可顯示smooth muscle α-actin 及myocardin 表現於頸動脈受傷後增加，而被atorvastatin 或 myocardin siRNA 抑制。結論：Myocardin 蛋白或myocardin mRNA 表現於頸動脈受傷模式下造成血管平滑肌肥厚時增加，以atorvastatin 或myocardin siRNA 治療可回復myocardin 對此血管平滑肌肥厚之不正常調控。

Background and purpose: The use of statin has been documented to be effective toinhibit vascular smooth muscle cell (VSMC) hypertrophy. Myocardin, a cardiac regulated gene,is up-regulated in VSMC hypertrophy. However, the effect of statin on myocardin expressiondue to balloon injury-induced carotid intimal hyperplasia is little known. Methods: To evaluatethe effect of statin on myocardin expression and VSMC hypertrophy, balloon injury to carotidartery of adult Sprague-Dawley rats was performed to induce VSMC hypertrophy. Atorvastatin(30 mg/kg) was given per day after surgery for 14 days. Results: Both myocardin mRNA andprotein increased significantly after balloon injury to carotid artery, which was inhibited by eithermyocardin small interfering RNA (siRNA) or atorvastatin. Increased intimal areas and decreasedlumen to intima ratios of carotid artery were noted after balloon injury, which was also inhibitedby myocardin siRNA and atorvastation. Increased immunohistochemical labelings of myocardinand smooth muscle (SM) actin in the VSMCs of carotid artery were observed and atorvastatinor myocardin siRNA again reversed the labelings. Conclusions: Both myocardin protein andmyocardin mRNA expressions were up-regulated in the rat model of balloon injury-inducedVSMC hypertrophy. Treatment with atorvastatin or myocardin siRNA is associated with a reversalof abnormal regulation of myocardin in the hypertrophic VSMC of carotid artery.