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氧化砷预防家兔血管损伤后再狭窄及其机理的研究

Effect of arsenic trioxide on inhibition of restenosis after rabbit vascular injury and its mechanism

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目的探讨应用三氧化二砷(As2O3)预防血管损伤后再狭窄的效果及其作用机理. 方法观察As2O3对培养兔血管平滑肌细胞 (VSMCs) 凋亡的影响.32只新西兰白兔随机分为2、4周实验组和对照组,分别10% As2O3 2.5 mg*Kg-1*d-1或等量生理盐水腹腔注射3天,应用球囊损伤左颈总动脉.处死动物取血管作形态学和免疫组化检测,并检查肝脏、肾脏组织学变化. 结果细胞形态学和DNA电泳梯形带证实,As2O3诱导培养VSMCs凋亡,与药物浓度和作用时间呈依赖性.与对照组相比,2-wk实验组血管内膜增殖面积显著减少(P<0.05),4-wk组内膜面积无明显差异;但2-, 4-wk组的管腔面积均有明显增大(P均<0.05).与对照组相比,实验组2-, 4-wk免疫组化显示bcl-2表达下调(P均<0.05),Bax表达上调 (P分别<0.01, 0.05),均与相对应的血管内膜增生受抑制,血管腔面积扩大相吻合. 结论 As2O3诱导VSMCs凋亡和有效预防实验性血管损伤后再狭窄,均与下调bcl-2和上调bax表达有关.

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Objective To investigate the effect and mechanism of arsenic trioxide (As2O3) on the prevention of restenosis after vascular injury. Methods Apoptosis induction of As2O3 on cultured rabbit vascular smooth muscle cells (VSMCs) in vitro was observed. Thirty-two New Zealand white rabbits were randomly divided into 2-and 4-wk study groups, and their controls. 10% As2O3 at 2.5 mg*Kg-1*d-1 or 0.9% sodium chloride was intraperitoneally infused for 3 days before left common carotid arteries were denudated with a balloon. After denudation 2-and 4-wk animals were sacrificed for morphometry and immunohistochemical studies on carotid arteries, and for histopathology on liver and kidney. Results It was shown via cellular morphology and DNA fragments in electrophoresis that promotion of As2O3 on cultured vascular smooth muscle cell apoptosis was dependent upon its concentration and duration. Compared with the control animals, the mean vascular intimal proliferation areas were reduced in 2-wk study animals (P<0.05) and no difference was shown in 4-wk (P>0.05), while the mean vascular luminal areas were all enlarged in both study groups (all P<0.05). The downregulated bcl-2 expression (all P<0.05 in 2-and 4-wk) and the upregulated bax expression (P<0.01 in 2-wk; P<0.05 in 4-wk) were detected by immunohistochemistry, in comparison with control groups. Gene bcl-2 and bax protein expression were consistent with the suppression of intimal proliferation and the enlargement of luminal areas in corresponding sections. Conclusion As2O3 induces apoptosis of VSMCs and inhibits experimental restenosis effectively after artery injury, via downregulation of bcl-2 and upregulation of bax expression.

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