Yang Ning, Dong Bo, Yang Jinyu, Li Yang, Kou Lu, Liu Yue, Qin Qin
Department of Cardiovascular, Tianjin Chest Hospital, Tianjin - China.
Arq Bras Cardiol. 2018 Oct;111(4):562-568. doi: 10.5935/abc.20180163. Epub 2018 Sep 21.
Restenosis after percutaneous coronary intervention in coronary heart disease remains an unsolved problem. Clusterin (CLU) (or Apolipoprotein [Apo] J) levels have been reported to be elevated during the progression of postangioplasty restenosis and atherosclerosis. However, its role in neointimal hyperplasia is still controversial.
To elucidate the role Apo J in neointimal hyperplasia in a rat carotid artery model in vivo with or without rosuvastatin administration.
Male Wistar rats were randomly divided into three groups: the control group (n = 20), the model group (n = 20) and the statin intervention group (n = 32). The rats in the intervention group were given 10mg /kg dose of rosuvastatin. A 2F Fogarty catheter was introduced to induce vascular injury. Neointima formation was analyzed 1, 2, 3 and 4 weeks after balloon injury. The level of Apo J was measured by real-time PCR, immunohistochemistry and western blotting.
Intimal/medial area ratio (intimal/medial, I/M) was increased after balloon-injury and reached the maximum value at 4weeks in the model group; I/M was slightly increased at 2 weeks and stopped increasing after rosuvastatin administration. The mRNA and protein levels of Apo J in carotid arteries were significantly upregulated after rosuvastatin administration as compared with the model group, and reached maximum values at 2 weeks, which was earlier than in the model group (3 weeks).
Apo J served as an acute phase reactant after balloon injury in rat carotid arteries. Rosuvastatin may reduce the neointima formation through up-regulation of Apo J. Our results suggest that Apo J exerts a protective role in the restenosis after balloon-injury in rats.
冠心病经皮冠状动脉介入治疗后的再狭窄仍是一个未解决的问题。据报道，在血管成形术后再狭窄和动脉粥样硬化进展过程中，簇集素（CLU）（或载脂蛋白[Apo]J）水平会升高。然而，其在新生内膜增生中的作用仍存在争议。
在大鼠颈动脉体内模型中，阐明Apo J在有或无瑞舒伐他汀给药情况下对新生内膜增生的作用。
将雄性Wistar大鼠随机分为三组：对照组（n = 20）、模型组（n = 20）和他汀干预组（n = 32）。干预组大鼠给予10mg/kg剂量的瑞舒伐他汀。插入2F Fogarty导管诱导血管损伤。在球囊损伤后1、2、3和4周分析新生内膜形成情况。通过实时PCR、免疫组织化学和蛋白质印迹法测量Apo J水平。
球囊损伤后，模型组内膜/中膜面积比（内膜/中膜，I/M）增加，并在4周时达到最大值；给予瑞舒伐他汀后，I/M在2周时略有增加，之后不再增加。与模型组相比，给予瑞舒伐他汀后颈动脉中Apo J的mRNA和蛋白水平显著上调，并在2周时达到最大值，早于模型组（3周）。
Apo J在大鼠颈动脉球囊损伤后作为急性期反应物发挥作用。瑞舒伐他汀可能通过上调Apo J减少新生内膜形成。我们的结果表明，Apo J在大鼠球囊损伤后的再狭窄中发挥保护作用。
