【摘要】：目的研究菲牛蛭素對載脂蛋白E基因敲除(ApoE~(-/-))小鼠動脈粥樣硬化及斑塊的干預(yù)作用。方法按照體重將高脂飼料喂養(yǎng)的雄性ApoE~(-/-)小鼠隨機分為3組:模型組、對照組(給予辛伐他汀3mg·kg~(-1)·d~(-1)灌胃)和實驗組(給予菲牛蛭素400 U·kg~(-1)·d~(-1)腹腔注射);另設(shè)C57BL/6J小鼠為正常組(不予任何處理)。給藥10周后,全自動生化儀檢測各組小鼠血清三酰甘油(TG)、總膽固醇(TC)、低密度脂蛋白膽固醇(LDL-C)及高密度脂蛋白膽固醇(HDL-C)的水平,以免疫組化法檢測主動脈血管標(biāo)記物CD34蛋白、血管內(nèi)皮生長因子(VEGF)及血管內(nèi)皮生長因子受體(VEGFR-2)的表達(dá)。結(jié)果給藥后,模型組、對照組和實驗組血清TG分別為(1.57±0.12),(1.10±0.21),(0.95±0.20)mmol·L~(-1);這3組的TC分別為(19.93±2.24),(14.47±1.30),(11.90±2.38)mmol·L~(-1);這3組的LDL-C分別為(17.24±1.52),(13.94±1.46),(10.02±2.14)mmol·L~(-1);這3組的HDL-C分別為(4.05±1.81),(4.62±0.50),(3.38±0.24)mmol·L~(-1),與模型組相比,實驗組差異均有統(tǒng)計學(xué)意義(均P0.01)。模型組、對照組和實驗組的斑塊膠原相對含量分別為(21.48±2.44)%,(37.12±3.33)%,(51.60±2.47)%;這3組的CD34蛋白含量分別為(11.02±1.64)%,(6.82±0.66)%,(4.56±0.59)%;這3組的VEGF蛋白分別為(22.13±2.04)%,(16.20±0.65)%,(11.16±0.82)%;這3組的VEGFR-2蛋白表達(dá)分別為(17.90±0.73)%,(15.11±0.52)%,(10.56±0.60)%;與模型組相比,實驗組差異均有統(tǒng)計學(xué)意義(均P0.01)。結(jié)論菲牛蛭素可改善ApoE~(-/-)小鼠動脈粥樣硬化,穩(wěn)定粥樣斑塊,其機制可能與減少VEGF和VEGFR-2表達(dá)、抑制斑塊微血管新生有關(guān)。
[Abstract]:Objective to study the effect of phenanthrene on atherosclerosis and plaques in apolipoprotein E knockout (ApoE~ (- / -) mice. Methods male ApoE~ (- / -) mice fed with high fat diet were randomly divided into three groups according to body weight: model group, The control group (treated with simvastatin 3mg kg~ (- 1) d ~ (- 1) and the experimental group (treated with 400 U kg~ (- 1) d ~ (- 1) were given intraabdominal injection of phenanthrene (- 1) d ~ (- 1). C57BL/6J mice were also set as normal group (without any treatment). After 10 weeks of administration, the levels of serum triacylglycerol (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were measured by automatic biochemical instrument. The expression of aortic vascular marker CD34 protein, vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (VEGFR-2) was detected by immunohistochemistry. Results after administration, the serum TG of the model group, the control group and the experimental group were (1.57 鹵0.12), (1.10 鹵0.21), (0.95 鹵0.20) mmol 路L ~ (- 1), respectively. The TC of the three groups was (19.93 鹵2.24), (14.47 鹵1.30), (11.90 鹵2.38) mmol 路L ~ (- 1), respectively. The LDL-C of the three groups was (17.24 鹵1.52), (13.94 鹵1.46), (10.02 鹵2.14) mmol 路L ~ (- 1), respectively. The HDL-C of the three groups was (4.05 鹵1.81), (4.62 鹵0.50), (3.38 鹵0.24) mmol 路L ~ (- 1), which was significantly different from that of the model group (all P 0.01). In the model group, the relative contents of plaque collagen in the control group and the experimental group were (21.48 鹵2.44)%, (37.12 鹵3.33)% and (51.60 鹵2.47)%, respectively. The contents of CD34 protein in these three groups were (11.02 鹵1.64)%, (6.82 鹵0.66)%, (4.56 鹵0.59)%, and (22.13 鹵2.04)%, (16.20 鹵0.65)%, (11.16 鹵0.82)%, respectively. The expression of VEGFR-2 protein in the three groups was (17.90 鹵0.73)%, (15.11 鹵0.52)% and (10.56 鹵0.60)%, respectively, which was significantly different from that in the model group (all P 0.01). Conclusion phenanthrene can improve atherosclerosis and stabilize atherosclerotic plaques in ApoE~ (- / -) mice. The mechanism may be related to the decrease of VEGF and VEGFR-2 expression and the inhibition of plaque microvessel regeneration.
【作者單位】： 廣西醫(yī)科大學(xué)藥學(xué)院;廣西科學(xué)院生物研究所;南寧市動物疫病預(yù)防控制中心;廣西醫(yī)科大學(xué)第二附屬醫(yī)院藥學(xué)部;
【基金】：廣西科學(xué)研究與技術(shù)開發(fā)基金資助項目(桂科攻0424008-2F)
【分類號】：R285.5

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