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目的研究细胞间黏附分子-1(ICAM-1)和新生血管在动脉粥样硬化中的表达情况的相关性研究。方法 8周龄Apo E-/-小鼠给予高脂饮食喂养分别至16,24,32周龄,建立代表动脉粥样硬化病变自起始至脂肪纹、纤维斑块及粥样斑块形成不同病变阶段的实验动物模型,取小鼠血清,全自动生化分析仪测定总胆固醇(TC)、低密度脂蛋白胆固醇(LDL)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL),通过免疫组化的方法检测动脉粥样硬化斑块内ICAM-1的表达量。用CD31抗体免疫组化标记新生血管。结果随着周龄增加,TC和LDL逐步增加,8,16,24,32周龄小鼠TC分别为(1.48±0.13),(3.56±0.25),(8.95±0.33),(12.23±0.58)mmol·L~(-1),LDL分别为(0.65±0.06),(2.36±0.18),(4.19±0.31),(5.64±0.55)mmol·L~(-1),与8周龄相比,差异均有统计学意义(P<0.05)。ICAM相对表达量随周龄逐步增加,8,16,24,32周龄小鼠ICAM-1分别为0.05±0.02,1.25±0.35,2.56±0.46,5.23±0.17;8,16,24,32周龄小鼠新生血管数分别为2.12±0.56,7.17±2.64,12.86±3.72,16.78±3.52,与8周龄相比,差异均有统计学意义(P<0.05)。ICAM-1与新生血管呈正相关(y=2.79 x+3.40,r2=0.927 9)。结论动脉粥样进展过程中,ICAM-1与新生血管表达量逐步增加,ICAM-1的表达增加可能是导致动脉粥样新生血管增加的原因。
Objective To study the correlation between the expression of intercellular adhesion molecule-1 (ICAM-1) and neovascularization in atherosclerosis. Methods Eight-week-old Apo E - / - mice were given a high-fat diet for 16, 24, and 32 weeks of age, respectively. A representative atherosclerotic lesion was established from initial onset to fatty streaks. Fiber plaque and plaque formation were different (TC), low density lipoprotein cholesterol (LDL), triglyceride (TG) and high density lipoprotein cholesterol (HDL) were measured by using mouse serum and automatic biochemical analyzer. Immunohistochemistry was used to detect the expression of ICAM-1 in atherosclerotic plaque. CD31 antibody was used to immunohistochemically label neovascularization. Results TC and LDL gradually increased with the increase of week age. The TC of 8, 16, 24 and 32 week old mice were (1.48 ± 0.13), (3.56 ± 0.25), (8.95 ± 0.33) and (12.23 ± 0.58) (0.65 ± 0.06), (2.36 ± 0.18), (4.19 ± 0.31) and (5.64 ± 0.55) mmol·L -1, respectively, compared with those of 8 weeks , The differences were statistically significant (P <0.05). The relative expression level of ICAM gradually increased with age, ICAM-1 of mice of 8, 16, 24 and 32 weeks were 0.05 ± 0.02, 1.25 ± 0.35, 2.56 ± 0.46 and 5.23 ± 0.17 respectively; 8, 16, 24 and 32 weeks The number of neovascularization in mice was 2.12 ± 0.56, 7.17 ± 2.64, 12.86 ± 3.72 and 16.78 ± 3.52, respectively. Compared with 8 weeks, the difference was statistically significant (P <0.05). ICAM-1 was positively correlated with neovascularization (y = 2.79 x + 3.40, r2 = 0.927 9). Conclusions During the process of atherosclerosis, the expression of ICAM-1 and neovascularization gradually increase. The increased expression of ICAM-1 may be responsible for the increase of atherosclerotic neovascularization.