Nose M, Ito M, Koide T, Terawaki K, Ogihara Y
Department of Pharmacognosy and Plant Chemistry, Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
Planta Med. 1996 Oct;62(5):410-2. doi: 10.1055/s-2006-957927.
The effects of 18 alpha,beta-glycyrrhetinic acid (18 alpha,beta-GA) on the hormonal induction of tyrosine aminotransferase (TAT) in rat primary cultured hepatocytes were investigated. Dexamethassone or glucagon used alone caused an increase in enzyme activity, and in combination their effects were additive. In the 18 beta-GA hepatocytes pretreated for 6 h, the dexamethasone-induced increase in the enzyme activity was slightly reduced in a dose-independent manner, and the glucagon-induced increase and the combined effects of these two inducers were significantly reduced in a dose-dependent manner. On the other hand, 18 alpha-GA, which was the isomer of 18 beta-GA, exerted no influence on the hormonally mediated increase in enzyme activity. Moreover, 18 beta-GA reduced the glucose release induced by glucagon in a dose-dependent manner and 18 alpha-GA did not. These results suggested that 18 beta-GA reduced the glucagon-mediated cell response in rat hepatocytes.
研究了18α,β-甘草次酸(18α,β-GA)对大鼠原代培养肝细胞中酪氨酸转氨酶(TAT)激素诱导作用的影响。单独使用地塞米松或胰高血糖素会导致酶活性增加,二者联合使用时其作用具有相加性。在预先用18β-GA处理6小时的肝细胞中,地塞米松诱导的酶活性增加以剂量非依赖性方式略有降低,而胰高血糖素诱导的增加以及这两种诱导剂的联合作用则以剂量依赖性方式显著降低。另一方面,18α-GA作为18β-GA的异构体,对激素介导的酶活性增加没有影响。此外,18β-GA以剂量依赖性方式降低了胰高血糖素诱导的葡萄糖释放,而18α-GA则没有。这些结果表明,18β-GA降低了大鼠肝细胞中胰高血糖素介导的细胞反应。