Heiman A S, Lee H J
Steroids. 1981 Oct;38(4):365-73. doi: 10.1016/0039-128x(81)90071-4.
Steroid acid esters, synthesized by modifying the 17-ketol side chain of prednisolone, were tested for their in vitro ability to stabilize heavy mitochondrial lysosomes prepared from rat liver. Membrane stabilization was determined by assessing capability of steroids to decrease extrusion of the marker enzymes (acid phosphatase, beta-glucuronidase and aryl sulfatase) from lysosomes incubated in hypo-osmotic sucrose-Tris acetate buffer. Results indicated that prednisolone (1) significantly inhibited the lysosomal release of acid phosphatase as did the new anti-inflammatory steroid, methyl 20-dihydroprednisolonate. Methyl prednisolonate exhibited weak membrane stabilization capacities and 20-dihydroprednisolonic acid, a metabolic product of methyl 20-dihydroprednisolonate, showed virtually no membrane stabilization.
通过修饰泼尼松龙的17 - 酮醇侧链合成的甾体酸酯，对其在体外稳定从大鼠肝脏制备的重线粒体溶酶体的能力进行了测试。通过评估甾体降低在低渗蔗糖 - 三乙酸缓冲液中孵育的溶酶体中标记酶（酸性磷酸酶、β - 葡萄糖醛酸酶和芳基硫酸酯酶）外排的能力来确定膜稳定性。结果表明，泼尼松龙（1）显著抑制酸性磷酸酶从溶酶体的释放，新的抗炎甾体20 - 二氢泼尼松龙甲酯也有此作用。甲泼尼龙表现出较弱的膜稳定能力，而20 - 二氢泼尼松龙甲酯的代谢产物20 - 二氢泼尼松龙酸几乎没有膜稳定作用。
