Zhang Q Y, He W, Dunbar D, Kaminsky L
Wadsworth Center, New York State Department of Health, Albany 12201-0509, USA.
Biochem Biophys Res Commun. 1997 Apr 28;233(3):623-6. doi: 10.1006/bbrc.1997.6508.
We have examined the inducibility of CYP1A1 by beta-naphthoflavone (BNF) in a rat intestinal epithelial cell line, IEC-18, and the associated interaction between cAMP and BNF. CYP1A1 was not constitutively expressed in IEC-18 cells. Upon treatment with BNF, CYP1A1 RNA, protein, and microsomal 7-ethoxyresorufin O-deethylase activity were detected. Treatment with dibutyryl cAMP resulted in a 2-fold increase in the extent of induction at both RNA and protein levels, with corresponding increases in CYP1A1 enzymatic activity. These results support the involvement of protein kinase A in Ah receptor-mediated induction of CYP1A1 and provide an in vitro model for further studies on the mechanisms underlying regional and cellular differences in the regulation of CYP1A1 gene expression in the small intestine.
我们研究了β-萘黄酮（BNF）在大鼠肠上皮细胞系IEC-18中对CYP1A1的诱导能力，以及环磷酸腺苷（cAMP）与BNF之间的相关相互作用。CYP1A1在IEC-18细胞中不是组成性表达的。用BNF处理后，检测到CYP1A1 RNA、蛋白质和微粒体7-乙氧基异吩恶唑酮O-脱乙基酶活性。用二丁酰环磷腺苷（dibutyryl cAMP）处理导致RNA和蛋白质水平的诱导程度增加了2倍，同时CYP1A1酶活性相应增加。这些结果支持蛋白激酶A参与芳烃受体介导的CYP1A1诱导，并为进一步研究小肠中CYP1A1基因表达调控的区域和细胞差异的潜在机制提供了一个体外模型。
