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目的:观察苯磺酸左旋氨氯地平对新西兰兔腹主动脉球囊内皮损伤术后动脉粥样硬化(AS)的影响,从抗炎和稳定斑块的角度探讨相关机制。方法:42只新西兰兔随机分为假手术组、模型组、左旋氨氯地平组以及瑞舒伐他汀组。模型采用高脂饮食联合腹主动脉球囊内皮损伤术制作。ELISA法检测各组术前与术后8周的血脂、血管炎症性及斑块稳定性相关指标,如超敏C反应蛋白(hs-CRP)、脂蛋白磷脂酶A2(Lp-PLA2)以及1型纤溶酶原激活物抑制物(PAI-1),术后8周处死后取腹主动脉病变组织,行HE染色分析斑块厚度及内膜增生系数(IHI)以及免疫组织化学法检测斑块内金属基质蛋白酶(MMP-3)表达。结果:左旋氨氯地平组血清低密度脂蛋白胆固醇(LDL-C)水平较模型组有降低趋势(16.24mmol/L∶19.41mmol/L,P=0.08)。左旋氨氯地平组的腹主动脉斑块厚度、IHI与模型组无显著性差异(313μm∶405μm、0.68∶0.66,均P>0.05),而瑞舒伐他汀组的斑块厚度、IHI明显低于模型组(273.75μm∶405.93μm、0.52∶0.68,均P<0.05)。左旋氨氯地平组的血清hs-CRP、Lp-PLA2以及PAI-1水平与模型组无明显差异(P>0.05),而左旋氨氯地平组斑块内MMP-3阳性表达面积百分比显著小于模型组(52.45%∶70.84%,P<0.05)。结论:左旋氨氯地平具有降低血清LDL-C趋势,对抑制兔腹主动脉球囊内皮损伤术后的内膜增生无明显作用,但可通过抑制斑块内MMP-3的表达从而增加斑块稳定性。
OBJECTIVE: To observe the effect of levoamlodipine besylate on atherosclerosis (AS) after balloon injury of abdominal aorta in New Zealand rabbits and to explore its mechanism from anti-inflammation and stable plaque. Methods: Forty-two New Zealand rabbits were randomly divided into sham operation group, model group, levamlodipine group and rosuvastatin group. Model using high-fat diet combined with abdominal aortic balloon endothelial injury surgery. Serum lipids, vascular inflammation and plaque stability related indexes such as hs-CRP, Lp-PLA2 and Lp-PLA2 were measured by ELISA before and 8 weeks after operation. (PAI-1) was injected into the abdominal aorta and the abdominal aorta lesions were sacrificed 8 weeks after the operation. The plaque thickness, intimal hyperplasia index (IHI) and immunohistochemical staining Blocking of matrix metalloproteinases (MMP-3). Results: The LDL-C level of L-amlodipine group was lower than that of model group (16.24mmol / L, 19.41mmol / L, P = 0.08). The thickness of abdominal aortic plaque in levamlodipine group, IHI and the model group had no significant difference (313μm: 405μm, 0.68:0.66, both P> 0.05), while rosuvastatin group plaque thickness, IHI was significantly lower The model group (273.75μm: 405.93μm, 0.52: 0.68, P <0.05). The levels of hs-CRP, Lp-PLA2 and PAI-1 in levamlodipine group were not significantly different from those in model group (P> 0.05), while the area of positive expression of MMP-3 in levamlodipine group was significantly lower than that of model group Group (52.45%: 70.84%, P <0.05). CONCLUSION: L-amlodipine has a trend of decreasing serum LDL-C and has no effect on inhibiting intimal hyperplasia of rabbit abdominal aortic balloon injury, but it can increase plaque by inhibiting MMP-3 expression in plaque stability.