3,4,5,6-四羟基口山酮抑制ApoE基因缺陷小鼠动脉粥样硬化形成及机制  

Suppression of 3,4,5,6-tetrahydroxyxanthone on atherogenesis and its mechanisms in apolipoprotein E deficient mice

作　　者：肖红波[1] 李年生[1] 贾素洁[1] 杨芝春[1] 郭韧[1] 胡高云[2] 李元建[1] 

机构地区：[1]中南大学药学院药理学系,长沙410078 [2]中南大学药学院药物化学系,长沙410013

出　　处：《国际病理科学与临床杂志》2006年第3期185-189,F0003,共6页Journal of International Pathology and Clinical Medicine

摘　　要：目的:研究3,4,5,6-四羟基口山酮抑制ApoE基因缺陷小鼠动脉粥样硬化(AS)形成的机制及其与内源性一氧化氮合酶(NOS)抑制剂非对称性二甲基精氨酸(ADMA)的关系。方法:32只小鼠分为4组(n=8):正常对照组(C57BL/6 J小鼠,等体积溶媒灌胃);模型组(ApoE基因缺陷小鼠,等体积溶媒灌胃);低剂量口山酮组[ApoE基因缺陷小鼠,口山酮10 mg/(kg.d)灌胃];高剂量口山酮组[ApoE基因缺陷小鼠,口山酮20 mg/(kg.d)灌胃];检测主动脉脂质斑块面积、血脂、红细胞变形性和血浆ADMA的水平。结果:与模型组比较,口山酮可以显著降低血浆ADMA水平和斑块面积,降低血浆总胆固醇(TC)、血浆总甘油三酯(TG)、血浆低密度胆固醇(LDL-C),显著升高血浆高密度胆固醇(HDL-C)和改善红细胞变形性。结论:3,4,5,6-四羟基口山酮具有抗AS作用,其作用机制与改善脂质代谢和降低血浆ADMA的水平有关。Objective To investigate the effect of 3,4,5,6-tetrahydroxyxanthone on atherogenesis in apolipoprotein E deficient mice and the relationship with endogenous nitric oxide synthase inhibitor. Methods Thirty-two mice were divided into 4 groups （ n = 8 ） ： C57BL/6J mice control group, Apo- E^-/- mice group, low dose xanthone-treated group [ 10 mg/（ kg· d） ], high dose xanthone-treated group [ 20 mg/（ kg · d）]. Atherosclerotic lesion area, blood lipids, erythrocyte deformability, and plasma asymmetric dimethylarginine （ADMA） level were determined. Results 3,4,5,6-tetrahydroxyxanthone significantly diminished the area of atherosclerotic lesion, decreased plasma total cholesterol （TC）, low density lipoprotein cholesterol（LDL-C） and triglyceride（ TG）, and increased plasma high density lipoprorein cholesterol（HDL-C）. 3,4,5,6-tetrahydroxyxanthone also decreased ADMA level and improved erythrocyte deformability. Conclusion 3,4,5,6-tetrahydroxyxanthone has the antiatherosclerotic effect, which may be related with the reduction of asymmetric dimethylarginine level.

关 键 词：3 4 5 6-四羟基(口山)酮 动脉粥样硬化斑块 血脂 红细胞变形性 非对称二甲基精氨酸 APOE基因缺陷小鼠 

分 类 号：R543.5[医药卫生—心血管疾病]