Chang W C, Kao H C, Liu Y W
Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, R.O.C.
Biochem Pharmacol. 1995 Sep 28;50(7):947-52. doi: 10.1016/0006-2952(95)00217-n.
The effect of glucocorticoids on epidermal growth factor (EGF)-induced expression of 12-lipoxygenase in human epidermoid carcinoma A431 cells was studied. A significant suppression of the EGF-induced expression of 12-lipoxygenase was observed in cells pretreated with 1 microM dexamethasone for 2 hr. The same pretreatment for 8 hr resulted in 55 and 54% inhibition of EGF-induced 12-lipoxygenase activity and mRNA expression, respectively. Cortisol, but not sex and mineral steroids, had a similar inhibitory effect. The glucocorticoid antagonist RU486 completely blocked the inhibitory effect of dexamethasone, suggesting that the action of dexamethasone was mediated through the ligation of glucocorticoid receptors. The results indicated that pretreatment of A431 cells with glucocorticoids resulted in a down-regulation of the EGF-induced expression of 12-lipoxygenase at the mRNA and enzyme activity level, which was mediated through glucocorticoid receptor activation.
研究了糖皮质激素对人表皮样癌A431细胞中表皮生长因子（EGF）诱导的12-脂氧合酶表达的影响。在用1微摩尔地塞米松预处理2小时的细胞中，观察到EGF诱导的12-脂氧合酶表达受到显著抑制。相同的预处理8小时分别导致EGF诱导的12-脂氧合酶活性和mRNA表达抑制55%和54%。皮质醇而非性激素和盐皮质激素具有类似的抑制作用。糖皮质激素拮抗剂RU486完全阻断了地塞米松的抑制作用，表明地塞米松的作用是通过糖皮质激素受体的结合介导的。结果表明，用糖皮质激素预处理A431细胞会导致EGF诱导的12-脂氧合酶在mRNA和酶活性水平上的表达下调，这是通过糖皮质激素受体激活介导的。
