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目的探讨动脉易损斑块(VP)与血管平滑肌细胞(VSMC)凋亡的关系及卡维地洛稳定斑块的作用机制。方法将45只雄性日本大耳白兔随机分成5组,分别为正常对照组、卡维地洛组、美托洛尔组、单纯转染组和单纯拉伤组,每组9只。正常对照组给予普通饲料,其他组给予球囊损伤颈总动脉加高脂喂养,8周后,除单纯拉伤组,其他3组给予野生型p53基因转染颈总动脉,卡维地洛组和美托洛尔组分别加喂卡维地洛和美托洛尔,继续高脂饲料喂养4周;实验前、实验后8、12周分别测定血脂;实验结束后检测斑块VSMC凋亡率及bcl-2、bax、α平滑肌肌动蛋白(-αactin)的局部表达情况,并分析血管病理形态学。结果球囊损伤组均出现典型动脉粥样硬化斑块,与单纯转染组比较,美托洛尔组及卡维地洛组纤维帽厚度均明显增加,卡维地洛组更显著(P<0.01);卡维地洛和美托洛尔对血脂均无明显影响;卡维地洛组斑块中VSMC凋亡率、bax及bax/bcl-2比值下降,上调-αactin、bcl-2阳性表达(P<0.01)。结论卡维地洛稳定斑块作用优于美托洛尔,其机制可能在于卡维地洛除β受体阻断作用外还具有抑制VSMC凋亡的作用。
Objective To investigate the relationship between the vulnerable plaque (VP) and the apoptosis of vascular smooth muscle cells (VSMC) and the mechanism of action of carvedilol. Methods Forty-five male Japanese white rabbits were randomly divided into 5 groups: normal control group, carvedilol group, metoprolol group, simple transfection group and simple strain group. The normal control group was given normal feed, while the other groups were given balloon-inflated common carotid artery plus high-fat diet. After 8 weeks, the other three groups were given wild-type p53 gene for carotid artery and carvedilol group And metoprolol group were fed with carvedilol and metoprolol, respectively. The rats were fed with high-fat diet for 4 weeks. Lipids were measured before and 8 and 12 weeks after the experiment. The apoptosis rate and bcl -2, bax, α-actin (α-actin), and analyze vascular pathomorphology. Results The typical atherosclerotic plaque appeared in the balloon injury group. Compared with the simple transfection group, the thickness of the fibrin cap in the metoprolol group and the carvedilol group was significantly increased, and the carvedilol group was more significant (P < 0.01). Carvedilol and metoprolol had no significant effect on blood lipids; the apoptosis rate of VSMC in the carvedilol group decreased, the ratio of bax and bax / bcl-2 decreased, the expressions of -actin and bcl-2 were up-regulated (P <0.01). Conclusion Carvedilol is superior to metoprolol in stabilizing plaque. The possible mechanism is that carvedilol can inhibit the apoptosis of VSMC in addition to β-blockade.