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目的:观察氯吡格雷对兔髂腹动脉球囊损伤后内膜增生的影响和作用机制。方法:37只新西兰兔随机分为正常组、模型组、氯吡格雷组及阿托伐他汀组。高脂喂养加髂动脉内膜剥脱建立动脉粥样硬化模型。检测血脂和高敏C反应蛋白(hsCRP)。12周后观察动脉病理组织学改变并测量内膜、中膜厚度和面积,原位杂交检测血小板源性生长因子(PDGFmRNA)的表达,免疫组化测定凋亡基因Bcl-2和Bax的表达。结果:①模型组血清hs-CRP、髂动脉内膜厚度和面积、PDGFmRNA、凋亡基因Bcl-2/Bax比值较正常组显著增加(P<0.05,P<0.01);②氯吡格雷组血清hs-CRP、内膜厚度与面积、PDGFmRNA的表达、Bcl-2/Bax的比值小于模型组(P<0.05,P<0.01),血脂水平和模型组无明显差异;③氯吡格雷对上述指标的改变与阿托伐他汀无显著差异。结论:氯吡格雷降低炎症反应、抑制PDGFmRNA表达、促进细胞凋亡,减轻高脂和球囊损伤后动脉内膜增殖。
Objective: To observe the effect and mechanism of clopidogrel on intima hyperplasia after balloon injury in iliac artery. Methods: Thirty-seven New Zealand white rabbits were randomly divided into normal group, model group, clopidogrel group and atorvastatin group. Atherosclerosis model was established by hyperlipidemia and iliac artery dissection. Blood lipids and high-sensitivity C-reactive protein (hsCRP) were detected. The changes of arterial histopathology were observed after 12 weeks and the intima and media thickness and area were measured. The expression of platelet derived growth factor (PDGFmRNA) was detected by in situ hybridization. The expressions of Bcl-2 and Bax were detected by immunohistochemistry. Results: ① The hs-CRP, the thickness and area of the intima of iliac artery, the ratio of PDGFmRNA and Bcl-2 / Bax in model group were significantly higher than those in normal group (P <0.05, P <0.01) hs-CRP, intima thickness and area, the expression of PDGFmRNA and the ratio of Bcl-2 / Bax in the model group were significantly lower than those in the model group (P <0.05, P <0.01) There was no significant difference between atorvastatin and atorvastatin. Conclusion: Clopidogrel can reduce the inflammatory reaction, inhibit the expression of PDGFmRNA, promote apoptosis, and attenuate the intima proliferation after hyperlipidemia and balloon injury.