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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。
AIM: To investigate the mechanism of 3,4,5,6-tetrahydroxychitosan inhibiting the formation of atherosclerosis (AS) in ApoE-deficient mice and its relationship with the endogenous nitric oxide synthase (NOS) inhibitor asymmetry Sexual dimethylarginine (ADMA) relationship. Methods: 32 mice were divided into 4 groups (n = 8): normal control group (C57BL / 6 J mice, equal volume of vehicle); model group (ApoE gene deficient mice, Low dose oral ketone group [ApoE gene-deficient mice, oral administration of 10 mg / (kg.d) of oral ketone]; high dose oral ketone group [ApoE-deficient mice, oral ketone 20 mg / (kg. d) gavage]; detection of aortic plaque area, lipids, erythrocyte deformability and plasma ADMA levels. Results: Compared with the model group, oral ketone can significantly reduce the level of plasma ADMA and plaque area, lower plasma total cholesterol (TC), total triglyceride (TG), plasma low density cholesterol (LDL-C) High plasma high-density cholesterol (HDL-C) and improve red cell deformability. CONCLUSION: 3,4,5,6-Tetrahydroxysperoid has anti-AS effect and its mechanism is related to improving lipid metabolism and decreasing plasma ADMA level.