蒙药达日布-8对动脉粥样硬化兔内皮祖细胞的影响
发布时间：2018-08-31 17:20
【摘要】：目的:研究蒙药达日布-8对动脉粥样硬化(AS)模型兔内皮祖细胞(EPCs)数量的调节作用。方法:将60只雄性新西兰兔随机分成6组:空白对照(A)组、模型对照(B)组、辛伐他汀(C)组、达日布-8低剂量(D)组、达日布-8中剂量(E)组、达日布-8高剂量(F)组,每组10只,每天给相应饲料并灌胃相应药物,饲养12周。分别于第0、4、8、12周,禁食12h后,耳缘静脉取血,经密度梯度离心法分离细胞、培养、鉴定。结果:B组内膜斑块形成明显,镜下可见大量泡沫细胞、脂质沉积,斑块向血管腔内突入,中膜平滑肌细胞呈不规则增生,证明模型有效。经Dil-Ac-LDL和FITC-UEA-I双染色后,第12周,与A组比较,B组双阳性细胞数量减少(P0.01),与B组比较,F组双阳性细胞增多(P0.01)。经荧光双抗CD34、VEGFR-2联合EPCs表型双染色后,第8周,兔外周血EPCs数量不同程度的发生变化,但与B组比较,各给药组差异并不显著。灌胃至第12周时,与B组比较,C、E、F组EPCs数量均明显增多(P0.01)。结论:大剂量蒙药达日布-8可以通过动员体内EPCs达到防治AS的作用。
[Abstract]:Aim: to study the effect of Mongolian drug Dazibu-8 on the (EPCs) quantity of endothelial progenitor cells in atherosclerotic (AS) model rabbits. Methods: sixty male New Zealand rabbits were randomly divided into 6 groups: blank control group (A), model control group (B), simvastatin (C) group, Dazibu-8 low dose (D) group, Dazibu-8 medium dose (E) group, Dazibu-8 high dose (F) group (10 rats in each group). The rats were fed with feed and medicine daily for 12 weeks. After fasting for 12 hours, the blood was taken from the vein of the auricular margin. The cells were isolated by density gradient centrifugation, cultured and identified. Results in group B, a large number of foam cells and lipid deposits were observed in the intimal plaques. The plaque protruded into the vascular lumen, and the medial smooth muscle cells showed irregular proliferation, which proved that the model was effective. At the 12th week after Dil-Ac-LDL and FITC-UEA-I double staining, the number of double positive cells in group B was lower than that in group A (P0.01), and the number of double positive cells in group F was more than that in group B (P0.01). After fluorescence double antibody CD34,VEGFR-2 combined with EPCs phenotype double staining, the number of EPCs in peripheral blood of rabbits changed in different degrees at the 8th week, but there was no significant difference between each administration group and group B. Compared with group B, the number of EPCs in group C (P 0.01) was significantly higher than that in group B (P < 0.01). Conclusion: large dose of Mongolian drug Dazibu-8 can prevent and cure AS by mobilizing in vivo EPCs.
【作者单位】： 内蒙古医科大学;内蒙古阿拉善盟蒙医医院;内蒙古呼伦贝尔市蒙医医院;
【基金】：国家自然科学基金项目主任基金项目(No.81341114)~~
【分类号】：R29
本文编号：2215650
[Abstract]:Aim: to study the effect of Mongolian drug Dazibu-8 on the (EPCs) quantity of endothelial progenitor cells in atherosclerotic (AS) model rabbits. Methods: sixty male New Zealand rabbits were randomly divided into 6 groups: blank control group (A), model control group (B), simvastatin (C) group, Dazibu-8 low dose (D) group, Dazibu-8 medium dose (E) group, Dazibu-8 high dose (F) group (10 rats in each group). The rats were fed with feed and medicine daily for 12 weeks. After fasting for 12 hours, the blood was taken from the vein of the auricular margin. The cells were isolated by density gradient centrifugation, cultured and identified. Results in group B, a large number of foam cells and lipid deposits were observed in the intimal plaques. The plaque protruded into the vascular lumen, and the medial smooth muscle cells showed irregular proliferation, which proved that the model was effective. At the 12th week after Dil-Ac-LDL and FITC-UEA-I double staining, the number of double positive cells in group B was lower than that in group A (P0.01), and the number of double positive cells in group F was more than that in group B (P0.01). After fluorescence double antibody CD34,VEGFR-2 combined with EPCs phenotype double staining, the number of EPCs in peripheral blood of rabbits changed in different degrees at the 8th week, but there was no significant difference between each administration group and group B. Compared with group B, the number of EPCs in group C (P 0.01) was significantly higher than that in group B (P < 0.01). Conclusion: large dose of Mongolian drug Dazibu-8 can prevent and cure AS by mobilizing in vivo EPCs.
【作者单位】： 内蒙古医科大学;内蒙古阿拉善盟蒙医医院;内蒙古呼伦贝尔市蒙医医院;
【基金】：国家自然科学基金项目主任基金项目(No.81341114)~~
【分类号】：R29
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1 郑万华;蒙药"达日布-罕达"应用前景分析[J];中国民族医药杂志;2004年04期
，本文编号：2215650
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