Yang Feng-zhen, Zhou Jun, Li Wen-wen, Wang Fang, Wen Pu-yuan, Zhou Li, Wang Jian-gang, Zheng Xing-xing
Department of Medical Laboratory, Central South University, Changsha, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2012 Aug;40(8):684-9.
To observe the histopathological features, nuclear factor-κB (NFκB) 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.
Eight C57BL/6J mice fed with normal diet were used as control, 32 ApoE(-/-) mice and LDLR(-/-) mice were divided into normal diet and high-fat diet groups (n = 8 each). After 4 months, aorta was collected for morphologic (HE, Oil Red O, Von Kossa) and immunohistochemistry (nuclear factor-κB, IKB, macrophage surface molecule-3, α-smooth action protein) analysis.
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. NFκB and IKB expressions in high-fat diet group were significantly higher than the normal diet group (P < 0.05). Double-labeling of NFκB 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).
High-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.
观察载脂蛋白E(ApoE)和低密度脂蛋白受体(LDLR)基因敲除小鼠(ApoE(-/-)、LDLR(-/-))高脂饮食喂养下动脉粥样硬化斑块(AS)的组织病理学特征、核因子-κB(NFκB)和IκB表达以及钙沉积情况。
选取8只喂食正常饮食的C57BL/6J小鼠作为对照,将32只ApoE(-/-)小鼠和LDLR(-/-)小鼠分为正常饮食组和高脂饮食组(每组n = 8)。4个月后,采集主动脉进行形态学(苏木精-伊红染色、油红O染色、冯科萨染色)和免疫组织化学(核因子-κB、IκB、巨噬细胞表面分子-3、α-平滑肌肌动蛋白)分析。
高脂饮食喂养的ApoE(-/-)和LDLR(-/-)小鼠的AS程度明显比正常饮食喂养的小鼠严重,且ApoE(-/-)小鼠的AS比LDLR(-/-)小鼠更显著。高脂饮食组的NFκB和IκB表达明显高于正常饮食组(P < 0.05)。NFκB双标显示在平滑肌细胞中占主导表达。高脂饮食喂养的ApoE(-/-)小鼠的钙沉积明显多于正常饮食喂养的小鼠(P < 0.05),高脂饮食和正常饮食喂养的LDLR(-/-)小鼠的钙沉积相似(P > 0.05)。
高脂饮食通过上调NFκB和IκB表达以及钙沉积,促进ApoE(-/-)和LDLR(-/-)小鼠AS斑块的形成。