Trzaskos J M, Jonas M, Chen H W
Medical Products Department, E. I. du Pont de Nemours and Co., Inc., Wilmington, DE 19880-0400.
Biochem Biophys Res Commun. 1989 May 30;161(1):267-71. doi: 10.1016/0006-291x(89)91590-8.
The mRNA levels for HMG-CoA reductase were measured in Chinese hamster lung Dede cells or ovary CHO cells by Northern blot analysis. It was observed that 25-hydroxycholesterol decreased the level of reductase mRNA by 40 to 70% in a 6 hour treatment. Inclusion of cycloheximide in the culture prevented the decrease observed with 25-hydroxycholesterol alone. Pretreatment of cells with 25-hydroxycholesterol for 6 hours prior to cycloheximide addition reveals that the protein synthesis inhibitor can return the suppressed levels of reductase mRNA back to control levels. Thus, protein synthesis is required for 25-hydroxycholesterol dependent suppression of HMG-CoA reductase mRNA.
通过Northern印迹分析测定了中国仓鼠肺Dede细胞或卵巢CHO细胞中HMG-CoA还原酶的mRNA水平。观察到，在6小时的处理中，25-羟基胆固醇使还原酶mRNA水平降低了40%至70%。在培养物中加入放线菌酮可防止单独使用25-羟基胆固醇时观察到的降低。在加入放线菌酮之前，先用25-羟基胆固醇预处理细胞6小时，结果表明，这种蛋白质合成抑制剂可使被抑制的还原酶mRNA水平恢复到对照水平。因此，25-羟基胆固醇依赖性抑制HMG-CoA还原酶mRNA需要蛋白质合成。
