A part of low density lipoproteins (LDL) isolated from the blood of healthy subjects and patients with coronary atherosclerosis bind to a Sepharose-linked Ricinus communis agglutinin, a lectin that interacts specifically with galactose residues. Bound LDL can be replaced by galactose, but not other saccharide constituents of the LDL molecule (mannose, glucose, N-acetylglucosamine, sialic acid). Bound LDL subfraction has a 2-3-fold lower content of sialic acid as compared with unbound LDL. The blood content of desialylated LDL in atherosclerotic patients was about 3-fold higher (1.5- to 6-fold) than in healthy subjects. Desialylated LDL induced a 2- to 4-fold more intensive accumulation of total cholesterol in cultured human aortic intimal cells. Unbound LDL had no effect on intracellular deposition of lipids. It is suggested that the subfraction of desialylated LDL may be responsible for the atherogenicity of LDL isolated from blood of atherosclerotic patients.

译文

从健康受试者和冠状动脉粥样硬化患者的血液中分离出的一部分低密度脂蛋白 (LDL) 与琼脂糖连接的蓖麻凝集素结合,凝集素与半乳糖残基特异性相互作用。结合的LDL可以用半乳糖代替,但不能用LDL分子的其他糖类成分 (甘露糖,葡萄糖,N-乙酰葡萄糖胺,唾液酸) 代替。与未结合的LDL相比,结合的LDL亚组分的唾液酸含量低2-3倍。动脉粥样硬化患者的去唾液酸化LDL的血液含量比健康受试者高约3倍 (1.5至6倍)。去唾液酸化的LDL在培养的人主动脉内膜细胞中诱导了2至4倍的总胆固醇密集积累。未结合的LDL对脂质的细胞内沉积没有影响。建议去唾液酸化的LDL的亚组分可能是从动脉粥样硬化患者血液中分离出的LDL的致动脉粥样硬化性的原因。

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