Yang B, Cao L, Fang R Y, Gu Z P
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, China.
Zhongguo Yao Li Xue Bao. 1997 Jul;18(4):367-70.
To study the influence of DL111-IT on progesterone biosynthesis of cultured luteal cells (LC).
LC viability was assessed with trypan blue dye exclusion and progesterone concentration was measured with radioimmunoassay.
DL111-IT decreased the viability of LC after 24-h incubation, its ED50 being 7.7 (95% confidence limits: 7.1-8.5) mg.L-1. DL111-IT inhibited basal secretion of progesterone in a concentration-dependent manner, and 3 mg.L-1 decreased progesterone concentration by 25% vs control. DL111-IT 3 mg.L-1 also inhibited the stimulatory effect of forskolin (cAMP activator) 10 mumol.L-1 and pregnenolone [converted to progesterone by 3 beta-hydroxysteroid dehydrogenase-isomerase complex (3 beta-HSD)] 10 mumol.L-1 on progesterone production in cultured LC, and their inhibitory rates were 43% and 155%, respectively. At the same concentration, DL111-IT did not influence hCG-induced progesterone production.
DL111-IT inhibited progesterone synthesis by suppressing the conversion of pregnenolone to progesterone (inactivating 3 beta-HSD) and suppressed the activity of cAMP. DL111-IT 6-24 mg.L-1 decreased the viability of LC.
研究DL111-IT对培养的黄体细胞（LC）孕酮生物合成的影响。
用台盼蓝拒染法评估LC活力，用放射免疫分析法测定孕酮浓度。
孵育24小时后，DL111-IT降低了LC的活力，其半数有效剂量（ED50）为7.7（95%置信区间：7.1 - 8.5）mg·L⁻¹。DL111-IT以浓度依赖的方式抑制孕酮的基础分泌，3 mg·L⁻¹时孕酮浓度较对照组降低了25%。3 mg·L⁻¹的DL111-IT还抑制了10 μmol·L⁻¹的福斯可林（cAMP激活剂）和10 μmol·L⁻¹的孕烯醇酮[通过3β-羟基类固醇脱氢酶-异构酶复合物（3β-HSD）转化为孕酮]对培养的LC中孕酮生成的刺激作用，其抑制率分别为43%和155%。在相同浓度下，DL111-IT不影响人绒毛膜促性腺激素（hCG）诱导的孕酮生成。
DL111-IT通过抑制孕烯醇酮向孕酮的转化（使3β-HSD失活）来抑制孕酮合成，并抑制cAMP的活性。6 - 24 mg·L⁻¹的DL111-IT降低了LC的活力。
