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全反式维甲酸对兔颈动脉粥样硬化模型内膜增殖的影响
引用本文:郭英华,董果雄,王国栋,张社华,高立建.全反式维甲酸对兔颈动脉粥样硬化模型内膜增殖的影响[J].青岛大学医学院学报,2005,41(2):129-131.
作者姓名:郭英华  董果雄  王国栋  张社华  高立建
作者单位:青岛大学医学院附属医院心内科,山东,青岛,266003;青岛大学医学院实验中心
基金项目:董果雄(1956-),男,硕士,教授,硕士生导师,E-mail:qydgx@public.qd.cn.
摘    要:①目的观察全反式维甲酸(ATRA)对兔颈动脉粥样硬化模型内膜增殖的影响。②方法36只新西兰大白兔随机分为假手术组、对照组和ATRA治疗组;假手术组给予高脂饮食但手术不损伤颈动脉内膜,余操作同对照组;对照组给予高脂饮食加空气干燥损伤颈动脉内膜;ATRA治疗组在高脂饮食加空气干燥损伤颈动脉内膜的同时给予ATRA治疗,内膜损伤后1周和4周观察平滑肌细胞中增殖细胞核抗原(PCNA)和细胞周期素E(cyclin E)的表达及兔颈动脉内膜增殖的情况。③结果ATRA治疗组平滑肌细胞中的PCNA和cyclin E的表达较对照组明显减弱(F=7.65~8.89,q=4.27~10.33,P〈0.05、0.01);颈总动脉病变也较对照组轻微(t=4.330~5.042,P〈0.01)。④结论ATRA能抑制兔颈动脉内膜损伤后内膜增殖,其机制可能为通过抑制cyclin E的表达而抑制平滑肌细胞的增殖。

关 键 词:维甲酸  内皮  血管  动脉粥样硬化
文章编号:1672-4488(2005)02-0129-03
收稿时间:2004-08-18
修稿时间:2004年8月18日

EFFECTS OF ATRA ON INTIMAL PROLIFERATION IN INJURED CAROTID ARTERY IN RABBITS
Guo YingHua;Dong GuoXiong;Wang GuoDong;Zhang SheHua;Gao LiJian.EFFECTS OF ATRA ON INTIMAL PROLIFERATION IN INJURED CAROTID ARTERY IN RABBITS[J].Acta Academiae Medicinae Qingdao Universitatis,2005,41(2):129-131.
Authors:Guo YingHua;Dong GuoXiong;Wang GuoDong;Zhang SheHua;Gao LiJian
Abstract:Objective To examine the effects of ATRA on post-injury intima of rabbit carotid artery. Methods Thirty-six rabbits were randomly divided into three groups, sham-operation group, control group and ATRA-treated group. The rabbits in the sham-operation group were fed with cholesterol-enriched diet but their carotid artery intima were not injured; those in the control group were fed with cholesterol-enriched diet and their carotid artery intima were injured; those in the ATRA-treated group were fed with cholesterol-enriched diet supplemented by ATRA for four weeks and their carotid artery intima were iniured.The carotid arteries were harvested for histomorphometry observation and PCNA and cyclin E immunohistochemistry analysis one and four weeks after the operation. Results ATRA decreased atherosclerotic lesion in rabbits carotid artery intima and the expression of PCNA and cyclin E in smooth muscle cells. Conclusion ATRA treatment can inhibit atherosclerotic progression by inhibiting the proliferation of vascular smooth muscle cells. The mechanism may be related to inhibition of cyclin E in vascular smooth muscle cells.
Keywords:retinoic acid  endothelium  vascular  atherosclerosis
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