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本文研究离体培养动脉内皮细胞通过LDL受体结合、内移和降解脂蛋白(α)[lipopro-tein(a),Lp(α)]的作用.实验取第3～4代离体培养的动脉内皮细胞分为两组,对照组培养液中不加碘标的脂蛋白(a)[~(125)I—Lp(α)],实验组培养液中加~(125)I—Lp(α)最终浓度分别为0.25、0.5、1、10和50μg/ml.用γ计数器测定内皮细胞对Lp(α)的结合、内移和降解值,并测定内皮细胞的蛋白质量,以μg/mg细胞蛋白表示.结果随培养液中加进~(125)I—Lp(α)的浓度递增而增加,在10μg/ml浓度时最大的结合、内移和降解值分别是0.219、0.390和0.465μg/mg细胞蛋白;最大的结合率、内移率和降解率分别是2.19%、3.90%和4.65%.结果提示Lp(α)通过动脉内皮细胞LDL受体途径的摄取和降解作用是非特异性的.
In this study, we investigated the effects of lipoprotein (a) and lipopolypelin (Lp (α)) on endothelial cells cultured and cultured in vitro, Arterial endothelial cells were divided into two groups. In the control group, iodine-labeled lipoprotein (a) [~ (125) I-Lp (α) ) Final concentrations were 0.25, 0.5, 1, 10 and 50 μg / ml, respectively.The binding, internal migration and degradation of endothelial cells to Lp (α) were measured by γ counter and the protein content of endothelial cells was measured in μg / Protein.The results showed that the concentration of 125 I-Lp (α) increased with the increase of culture medium, and the maximum binding, internal migration and degradation values at the concentration of 10μg / ml were 0.219,0.390 and 0.465μg / The maximum binding rate, internal migration rate and degradation rate were 2.19%, 3.90% and 4.65%, respectively.The results suggested that the uptake and degradation of Lp (α) via the LDL receptor pathway of arterial endothelial cells were nonspecific.