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目的探讨阿托伐他汀钙及福辛普利在高血脂症下对动脉粥样硬化的干预作用。方法 40只雌性C57BL/6小鼠,于左侧颈总动脉外置入鞘管后随机分为对照组、阿托伐他汀钙组[10mg/(kg.d)]、福辛普利组[50mg/(kg.d)]和联合用药组[阿托伐他汀钙10mg/(kg.d)+福辛普利50mg/(kg.d)]4组,每组10只。各组小鼠均术后当日饲以高脂饮食,用药组根据小鼠体质量通过饮水途径饲以相关药物,对照组未进行药物干预。观察12周后,进行血清学指标检测并取双侧颈动脉标本行HE染色。结果 HE染色可见对照组小鼠左侧颈总动脉有明显动脉粥样硬化形成,对照组小鼠左侧颈总动脉内膜中层厚度(IMT)明显高于阿托伐他汀钙组、福辛普利组和联合用药组[分别为(2.77±2.87)比(0.05±0.01)、(0.08±0.05)、(0.06±0.01)mm]。与对照组相比,阿托伐他汀钙能明显降低血清总胆固醇、低密度脂蛋白胆固醇(LDL-C)和巨噬细胞集落刺激因子(M-CSF)水平[总胆固醇(1.43±0.30)比(2.64±0.46)mmol/L;LDL-C(0.18±0.13)比(0.92±0.17)mmol/L;M-CSF(191.0±34.0)比(225.9±36.1)ng/L;均P<0.05],升高一氧化氮合酶(NOS)含量[(42.2±1.9)比(39.9±1.3)U/mL,P=0.01];与对照组比较,福辛普利组总胆固醇和LDL-C水平虽未见明显变化,但M-CSF和超氧化物歧化酶(SOD)水平明显降低[M-CSF(199.7±34.7)比(225.9±36.1)ng/L;SOD(40.6±10.2)比(50.7±3.8)U/mL;均P<0.05],NOS含量升高[(42.8±2.8)比(39.9±1.3)U/mL,P<0.01],两种药物联合应用未见明显协同效应(P>0.05)。结论阿托伐他汀钙及福辛普利均能抑制实验小鼠动脉粥样硬化的形成;两种药物联合应用未见明显协同作用。福辛普利较阿托伐他汀钙更能明显抑制小鼠体内氧化应激反应。
Objective To investigate the effects of atorvastatin calcium and fosinopril on atherosclerosis in patients with hyperlipidemia. Methods 40 female C57BL / 6 mice were randomly divided into control group, atorvastatin calcium group [10mg / (kg · d)], fosinopril group [ 50 mg / (kg · d)] and combination group [atorvastatin calcium 10 mg / (kg · d) + fosinopril 50 mg / (kg · d)]. The mice in each group were fed a high-fat diet on the day after the operation. The medication group was fed with the relevant drugs through the drinking water route according to the body weight of the mice, and the control group received no drug intervention. After 12 weeks of observation, serological detection was performed and bilateral carotid arteries were stained with HE. Results HE staining showed that the common carotid arteries of the left common carotid arteries of mice in the control group had obvious atherosclerosis. The intima-media thickness (IMT) of left carotid artery in the control group was significantly higher than that of the atorvastatin calcium group, (2.77 ± 2.87 vs 0.05 ± 0.01, (0.08 ± 0.05) and (0.06 ± 0.01) mm, respectively] in the combination group and the combination group. Compared with the control group, atorvastatin calcium significantly decreased serum total cholesterol, low density lipoprotein cholesterol (LDL-C) and macrophage colony stimulating factor (M-CSF) levels [1.43 ± 0.30 (2.64 ± 0.46) mmol / L, LDL-C (0.18 ± 0.13) vs (0.92 ± 0.17) mmol / L and M-CSF (191.0 ± 34.0) vs (225.9 ± 36.1) ng / L, respectively; (42.2 ± 1.9) vs (39.9 ± 1.3) U / mL, P = 0.01]. Compared with the control group, the levels of total cholesterol and LDL-C in the fosinopril group were significantly higher than those in the control group The levels of M-CSF and superoxide dismutase (SOD) were significantly lower in M-CSF (225.9 ± 36.1) ng / L and (40.6 ± 10.2) (P <0.01). There was no significant synergistic effect between the two drugs (P <0.05), P <0.05] > 0.05). Conclusions Both atorvastatin calcium and fosinopril can inhibit the formation of atherosclerosis in experimental mice. There is no obvious synergistic effect between the two drugs. Fosinopril significantly inhibited oxidative stress in mice compared with atorvastatin calcium.