Objective To observe the expression of apolipoprotein E ( ApoE ) gene knocking out hyperlipidemia (HLP) in mice submandibular gland ultrastructure and upstream stimulating factor 1 (USF1). Methods Take 10 wild mice fed with normal feed as control group, 10 ApoE knockout mice fed with high fat as hyperlipidemia group. Six months after the model was set up, blood fat in orbital blood was tested. The submandibular gland tissues of the mice were observed by using light microscopy, electron microscopy and immunohistochemistry staining. Results Compared with the control group, the cholesterol, triglycerides and very low-density lipoprotein of high-fat group were significantly higher (P<0. 05). HE staining was observed, the acini of the submandibular glands in hyper-lipidemia group was atrophied obviously, and the cells were in disorder. Under electron microscopy, the subman-dibular gland cell mitochondria crests of mice in hyperlipidemia group were fractured, and rough endoplasmic retic-ulum cystically expanded, which was loose and messy. Immunohistochemical results showed that the USF1 expres-sion in hyperlipidemia group decreased; the difference in average optical density value and the control group was statistically significant ( P<0. 05 ) . Conclusion HLP can result in pathological changes in the mouse submandib-ular gland ultrastructure and reduction in USF1 expression.%目的 观察载脂蛋白 E ( ApoE )基因敲除高脂血症( HLP)对小鼠下颌下腺超微结构以及上游刺激因子 1 (USF1)表达影响. 方法 10只野生型小鼠予普通饲料喂养作为对照组,10只ApoE基因敲除子鼠予高脂饲料喂养作为高脂组. 造模6个月后,取眼眶血检测血脂;取小鼠下颌下腺组织分别进行光镜、电镜和免疫组织化学观察. 结果 与对照组比较,高脂组胆固醇、三酰甘油和极低密度脂蛋白含量明显升高( P<0. 05 ). HE染色观察到,高脂组小鼠下颌下腺的腺泡明显萎缩,细胞排列紊乱. 电镜下,可见高脂组小鼠导管上皮内线粒体嵴断裂,腺细胞内粗面内质网囊状扩张,结构松散零乱. 免疫组化显示,高脂组USF1表达下降;平均光密度值与对照组比较差异有统计学意义( P<0. 05 ).结论 HLP可导致小鼠下颌下腺超微结构出现病理改变, USF1表达减少.
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