论文部分内容阅读
在供咀嚼的烟草、糖果和药物中作为配料的甘草,其钠潴留作用正逐渐为人们所认识。这种明显的盐皮质激素作用源自甘草次酸(甘草中的一种活性成份)对11β-羟类固醇脱氢酸(一种在正常情况下通过把C_(11)羟基转移到酮上而使皮质醇失活的酶)的抑制。靠阻止皮质醇的失活,甘草增加盐皮质激素应答组织中的糖皮质激素浓度。结果,糖皮质激素占据盐皮质激素受体和产生盐皮质激素效应,表现为钠潴留的增加和高血压。我们要指出的是甘草次酸也抑制15-羟前列腺素脱氢酶和Δ~(13)-前列腺素还原酶,这两种酶在前列腺素E和F_(2α)的代谢中起着重要的作用。因而,甘草的生理作用基础比人们通常想像的要复杂。
The role of sodium retention in licorice as an ingredient in chewing tobacco, confectionery and medicine is gradually becoming known. This apparent mineralocorticoid action results from glycyrrhetinic acid (an active ingredient in licorice) against 11β-hydroxysteroid dehydrogenic acid (a product which is normally transfered to the ketone by the C 11 hydroxy group) Cortisol inactivated enzyme) inhibition. By preventing the inactivation of cortisol, licorice increases the glucocorticoid concentration in the mineralocorticoid responsive tissue. As a result, glucocorticoids occupy the mineralocorticoid receptor and produce a mineralocorticoid effect, manifested by an increase in sodium retention and hypertension. We will point out that glycyrrhetinic acid also inhibits 15-hydroxyproline dehydrogenase and Δ13 (13) -prostat reductase, both of which play an important role in prostaglandin E and F 2α metabolism effect. Therefore, the physiological role of licorice base than people usually think complex.