摘要
目的研究维生素E对高脂血症小鼠血管内皮细胞凋亡相关蛋白基因表达的影响。方法选择性成熟雄性ICR小鼠50只,随机分为A、B、C、D、E组,每组10只,A、B、C、D组高脂饲料喂养,其中B、C、D组同时灌胃不同浓度维生素E,E组普通饲料喂养,连续喂养4周后处死小鼠,取主动脉内皮细胞测定凋亡相关蛋白基因的表达及静脉血脂的浓度。结果 B、C、D组中动脉血管内皮细胞中Bax蛋白基因mRNA水平的表达量明显低于A组(P<0.05),但高于E组(P<0.05);B、C、D组中Bcl-2蛋白基因mRNA水平的表达量明显高于A组(P<0.05),但低于E组(P<0.05);Bax与Bcl-2基因mRNA水平的表达量之间为负相关;B、C、D组中静脉血清总胆固醇(TC)、甘油三酯(TG)明显低于A组(P<0.05),除D组TC外均高于E组(P<0.05)。结论维生素E能抑制高脂血症所导致的血管内皮细胞凋亡相关基因的表达并升高抗凋亡基因的表达,同时降低血脂。
Objective To study the effect of Vitamin E on apoptosis-related gene expressions of vascular endothelial cells in mice with hyperlipidemia. Methods Viripotent 50 male ICR mice were randomly divided into group A, B,C,D and E（ n = 10 each group）. The mice in group A,B,C and D were fed with high-fat food,and group B,C and D were lavaged with different concentrations of Vitamin E,while group E was fed with normal diet. All the mice were killed after being fed for four weeks,and the gene expressions of Bax and Bcl-2 in mRNA and the concentrations of triglyceride（ TG） and total cholesterol（ TC） in serum of aortic endothelial cells were detected. Results The Bax expressions of mRNA level in arterial endothelial cells in group B,C and D were significantly lower than that in group A（ P ＆lt; 0. 05）,and higher than that in group E（ P ＆lt; 0. 05）; the Bcl-2 expressions of mRNA level in group B,C and D were significantly higher than that in group A（ P ＆lt; 0. 05）,but lower than that in group E（ P ＆lt; 0. 05）; there was a negative correlation between gene expressions of Bax and Bcl-2 in mRNA; the concentrations of TG and TC in group B,C and D were significantly lower than those in group A（ P ＆lt; 0. 05）,and the concentrations were significantly higher than those in group E,except for the TC concentration in group D（ P ＆lt; 0. 05）. Conclusion VitE can inhibit the apoptosis-related gene expressions of vascular endothelial cells induced by hyperlipemia,heighten anti- apoptogenic expression and reduce blood fat level at the same time.
出处
《解放军医药杂志》
CAS
2013年第12期62-65,共4页
Medical & Pharmaceutical Journal of Chinese People’s Liberation Army
基金
辽宁省自然科学基金资助项目(201102244)
