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作 者:杨凤真[1] 周军[2] 李闻文[1] 王芳[1] 温蒲圆[2] 周丽[2] 王建刚 郑星星
机构地区:[1]中南大学湘雅医学院医学检验系,长沙410013 [2]湘雅三医院医学实验中心神经内科 [3]湘雅三医院医学实验中心心血管内科
出 处:《中华心血管病杂志》2012年第8期684-689,共6页Chinese Journal of Cardiology
摘 要:目的观察高脂饮食后载脂蛋白E(ApoE)和低密度脂蛋白受体(LDLR)基因敲除(ApoE-/-和LDLR-/-)小鼠动脉粥样硬化(As)斑块内的组织病理学特征、核因子-κB(NF-κB)及其抑制蛋白(IKB)的表达以及钙沉积变化,研究高脂饮食对ApoE。和LDLR-/-小鼠血管的影响及其作用机制。方法8只C57BL/6J小鼠为普食对照组,ApoE-/-和LDLR-/-小鼠分成普食和高脂饮食各两组,每组8只,连续喂养4个月。取各组小鼠主动脉进行苏木素一伊红染色、油红O染色和钙沉积检测,用免疫组织化学法观察As斑块内NFKB和IKB的表达水平,荧光双标法分析As斑块内NF-κ的表达与巨噬细胞和平滑肌细胞的相关关系。结果ApoE-/-和LDLR-/-小鼠各高脂饮食组As斑块均大于普食组,脂肪沉积多于普食组,NFκ和IKB的表达水平均显著高于普食组(P均〈0.05)。NFs:B主要表达于平滑肌细胞。ApoE-/-一小鼠高脂饮食组钙沉积反应明显大于其普食组(P〈0.05),但LDLR-/-小鼠高脂饮食组钙沉积反应与其普食组比较,差异无统计学意义(P〉0.05)。结论高脂饮食促进ApoEI/和LDLR-/-小鼠As斑块的形成,上调NFKB和IKB的表达水平,增加钙沉积反应,从而加剧J,血管壁损伤。Objective To observe the histopathological features, nuclear factor-KB (NFKB) and IKB expressions as well as calcium deposition of atherosclerosis plaques (AS) in apolipoprotein E (ApoE) and low density lipoprotein receptor (LDLR) knockout mice (ApoE-/-, LDLR /-fed high-fat diet. Methods Eight C57BL/6J mice fed with normal diet were used as cqatrol, 32 ApoE -/- mice and LDLR / mice were divided into normal diet and high-fat diet groups (n = 8 Bach). After 4 months, aorta was collected for morphologic (HE, Oil Red O, Von Kossa) and immunohisto^hemistry (nuclear factor-κB, IKB, macrophage surface molecule-3, α-smooth activor protein ) analysis.Results Degree of AS in ApoE -/- and LDLR / mice fed with high-fat diet were significantly severer than those fed with normal diet and AS was more significant in ApoE -/- mice than in LDLR / - mice. NFKB and IKB expressions in high-fat diet group were significantly higher than the normal diet group ( P 〈 0. 05 ) . Double-labeling of NFKB revealed dominant expression in smooth muscle cells. Calcium deposition was significantly more in ApoE -/ mice fed with high-fat diet than mice fed with normal diet (P 〈0. 05) and was similar in LDLR-/ mice fed with high and normal diet ( P 〉 0. 05 ). Conclusion High-fat diet contributes to the formation of AS plagues in ApoE / - and LDLR /- mice joined by upregulated NFKB and IKB expressions and calcium deposition.
分 类 号:R543.5[医药卫生—心血管疾病]
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