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目的 :观察血管紧张素转换酶抑制剂 (ACEI)雷米普利和血管紧张素Ⅱ (AngⅡ ) 1型受体拮抗剂氯沙坦对高胆固醇血症大鼠早期动脉粥样硬化 (AS)形成的影响 ,探讨肾素 血管紧张素系统 (RAS)致早期AS的机制。方法 :4 0只雄性SD大鼠随机分为正常对照 (NC)组 ,高脂 (HL)组 ,雷米普利 (Ram )组和氯沙坦 (Los)组。每组 10只 ,10周后比色法测血清一氧化氮 (NO)、丙二醛 (MDA)水平及超氧化物歧化酶 (SOD)活力 ,酶法测血胆固醇浓度 ;用免疫组化法检测主动脉血管壁增殖细胞核抗原 (PCNA)和核转录因子 (NFκB)及细胞间粘附分子 1(I CAM 1)表达水平 ;透射电镜观察主动脉形态结构 ,苏木精 伊红染色高倍视野下计数浸润于内膜的单核细胞数。结果 :Ram组和Los组血清NO浓度和SOD活力显著高于HL组 (P <0 .0 1) ,而MDA水平低于HL组 (P <0 .0 1) ,NFκB活化及ICAM 1表达水平 ,PCNA阳性细胞数和浸润的单核细胞数明显少于HL组 (P <0 .0 1) ,但这三组间血胆固醇浓度差异无显著性意义。Ram组和Los组主动脉内皮损伤明显轻于HL组。结论 :Ram和Los能缓解自由基损伤 ,抑制高胆固醇血症大鼠ICAM 1表达和单核细胞浸润 ,防止早期AS形成。
AIM: To observe the effects of losartan, an inhibitor of angiotensin converting enzyme inhibitor (ACEI) and angiotensin Ⅱ type 1 receptor antagonist on the formation of early atherosclerosis (AS) in hypercholesterolemic rats Influence, explore the renin angiotensin system (RAS) induced early AS mechanism. Methods: 40 male Sprague-Dawley rats were randomly divided into normal control (NC) group, high fat (HL) group, Ramipril group and Los group. (N = 10). Serum levels of nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured by enzyme-linked immunosorbent assay The expression of proliferating cell nuclear antigen (PCNA), nuclear factor kappa B (NFκB) and intercellular adhesion molecule 1 (I CAM 1) in aorta were detected by transmission electron microscopy. Count the number of infiltrating monocytes in the intima. Results: Serum NO concentration and SOD activity in Ram group and Los group were significantly higher than those in HL group (P <0.01), while MDA levels were lower in HL group than in HL group (P <0.01). NFκB activation and ICAM 1 expression , The number of PCNA positive cells and infiltrating monocytes were significantly less than those in HL group (P <0.01). However, there was no significant difference between the three groups in blood cholesterol levels. The aortic endothelial injury in Ram group and Los group was significantly lighter than that in HL group. Conclusion: Ram and Los can relieve free radical injury, inhibit ICAM-1 expression and monocyte infiltration in hypercholesterolemic rats and prevent the formation of early AS.