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目的观察阿司匹林对动脉粥样硬化(AS)家兔血管壁核因子-kB(NF-kB)-DNA 结合活性、环氧化酶-2(COX-2)蛋白表达、AS 斑块面积和血管内膜厚度的影响,探讨阿司匹林的抗 AS 作用机制。方法36只雄性新西兰大耳白兔被随机分为正常对照组(NC)、高脂对照组(HC)和阿司匹林组(HC+A)。实验结束时,分别用酶法、固相酶联免疫吸附实验、电泳移动迁移技术、免疫组化技术、形态学方法检测3组兔的血脂、高敏 C 反应蛋白(hs-CRP)水平、主动脉组织中 NF-kB-DNA 结合活性、COX-2蛋白表达及各组主动脉新生内膜厚度和 AS 斑块面积。结果 HC 与 HC+A 组的血脂和 hs-CRP 水平、NF-kB-DNA 结合活性、COX-2蛋白表达、动脉新生内膜厚度和粥样斑块面积均明显大于 NC 组(P<0.05～0.01);HC+A 组的血脂水平与 HC 组相比差异无统计学意义(P>0.05),但HC+A 与 HC 组的 hs-CRP 水平[(5.14±0.32)μg/ml vs(9.39±0.79)μg/ml,P<0.05]、NF-kB-DNA 结合活性[(14.6±2.7)μg/ml vs(32.4±4.7)μg/ml,P<0.05]、COX-2蛋白表达[(0.342±0.02 vs 0.572±0.061,P<0.05)]、血管新生内膜厚度[(165±24)μm vs(337±64)μm(P<0.05)]和 AS 斑块面积[(24.3±7.6)%vs(49.5±21.3)%,(P<0.05)]相比差异有统计学意义。结论阿司匹林可通过抑制 NF-kB-DNA 结合活性、降低 hs-CRP 水平、减弱 COX-2蛋白表达而发挥抗 AS 作用。
Objective To observe the effect of aspirin on NF-κB-DNA binding activity, cyclooxygenase-2 (COX-2) protein expression, AS plaque area and intravascular level in atherosclerotic rabbits Membrane thickness, explore the anti-AS mechanism of aspirin. Methods Thirty - six male New Zealand white rabbits were randomly divided into normal control group (NC), high fat control group (HC) and aspirin group (HC + A). At the end of the experiment, the levels of serum lipids, high-sensitivity C-reactive protein (hs-CRP) and the aorta were detected by enzymatic method, enzyme-linked immunosorbent assay, electrophoretic mobility shift assay, immunohistochemistry and morphological methods respectively. NF-kB-DNA binding activity, COX-2 protein expression and aortic neointimal thickness and AS plaque area in each group. Results The levels of serum lipids and hs-CRP, NF-kB-DNA binding activity, COX-2 protein expression, arterial neointimal thickness and atheroma plaque area in HC and HC + A group were significantly higher than those in NC group (P <0.05 ~ 0.01). The level of hs-CRP in HC + A and HC group was significantly higher than that in HC group [(5.14 ± 0.32) μg / ml vs (9.39 (P <0.05), and the expression of COX-2 protein [(P <0.05) (165 ± 24) μm vs (337 ± 64) μm (P <0.05)] and AS plaque area [(24.3 ± 7.6) % vs (49.5 ± 21.3)%, (P <0.05)] compared with the difference was statistically significant. Conclusion Aspirin can play an anti-AS effect by inhibiting NF-kB-DNA binding activity, decreasing hs-CRP level and decreasing COX-2 protein expression.