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为了研究高密度脂蛋白 3介导大鼠腹腔巨噬细胞内胆固醇流出的机理 ,用N -乙酰咪唑修饰高密度脂蛋白 3,阻断其与细胞表面受体的结合 ,观察细胞内胆固醇流出。用异硫氰酸荧光素酯标记高密度脂蛋白 3,示踪其在细胞内的代谢。结果发现牛血清白蛋白 (对照组 )介导 2 .87%细胞内胆固醇流出 ,高密度脂蛋白 3组和N -乙酰咪唑 -高密度脂蛋白 3组分别为 40 .6 8%和 8.6 9%。异硫氰酸荧光素酯 -高密度脂蛋白 3与细胞在 37℃共育 3h后 ,细胞内吞荧光强度占结合的 6 5 .0 % ,细胞在 37℃继续培养 2h后 ,细胞释放的荧光强度占内吞的 78.4% ,并且内吞和释放的荧光强度均主要存在于三氯醋酸沉淀部分。结果提示高密度脂蛋白 3通过与细胞表面受体作用进入细胞 ,在细胞内不经过溶酶体途径降解 ,而是接受细胞内胆固醇后通过逆胞饮形式释放到细胞外
In order to investigate the mechanism of high density lipoprotein 3 - mediated cholesterol efflux in rat peritoneal macrophages, high - density lipoprotein 3 was modified with N - acetylimidazole to block its binding to cell surface receptors and to observe intracellular cholesterol efflux. High-density lipoprotein 3 was labeled with fluorescein isothiocyanate and its metabolism in the cells was observed. Bovine serum albumin (control group) was found to mediate 2.87% intracellular cholesterol efflux, 40.68% and 8.69%, respectively, in the high-density lipoprotein-3 and N-acetylcysteamine- . Fluorescein isothiocyanate-HDL-3 incubated with cells at 37 ℃ for 3h, the fluorescence intensity of endocytic cells accounted for 65.5% of the binding, the cells were incubated at 37 ℃ for 2h, the fluorescence of the cells The intensity accounted for 78.4% of endocytosis, and the endocytosis and release of fluorescence intensity are mainly present in the trichloroacetic acid precipitation part. The results suggest that high density lipoprotein 3 enters the cell through the interaction with the cell surface receptor and is not degraded in the cell through the lysosomal pathway but is released into the cell through the counterpulteration after receiving intracellular cholesterol