中文摘要：

目的探讨滋养层细胞糖代谢障碍对MLN64基因表达和胎盘激素代谢的影响及小檗碱、薯芋皂甙等药物对MLN64 mRNA表达的调节作用。方法取妊娠8-12周胎盘绒毛组织，从中分离出滋养细胞进行体外培养。培养48～72h后用Wortmaninn诱导细胞糖代谢发生异常，作为模型组（WT组），同时设立空白对照组（N组）。然后用小檗碱（B组）、薯芋皂甙（S组）、曲格列酮（T组）分别进行处理。采用RT—PCR检测细胞MLN64 mRNA的表达；化学发光法检测每组上清中孕酮、雌二醇水平；放射免疫法检测胎盘泌乳素（HPL）、人绒毛膜促性腺激素（p—HCG）水平。结果（1）WT组MLN64 mRNA的表达较N组下降了26．91％，B组和T组MLN64 mRNA的表达较WT组分别增加了69．93％和53．98％。（2）干预后T组雌激素和孕酮水平[分别为（143±19）pg／ml和（2．42±1．43）ng／ml]与WT组[（110±22）pg／ml和（0．78±0．42）g／ml]比较，差异有统计学意义（P〈0．05）。结论（1）滋养细胞糖代谢障碍能使MLN64 mRNA表达下降，可能影响甾体激素合成的限速步骤。小檗碱和曲格列酮能上调MLN64 mRNA表达，且二者作用相当；（2）除曲格列酮外，其他药物对胎盘激素分泌的影响不显著。

英文摘要：

Objective To discuss the effect of trophocytes saccharometabolism disorders on MLN64 gene expression and placental hormone metabolism, and the accommodation of Berberine and Dioscin on MLN64 mRNA expression. Methods Trophocytes were isolated from placenta villi of 8 - 12 - week pregnant women to culture in vitro. Wortmaninn was used to induce saccharometabolism disorders （WT group）, and at the same time control group （N group） was set up. And then Berberine （B group）, Dioscin （S group） and Troglitazone （T group） were used respectively. MLN64 mRNA expression was determined by RT - PCR, the levels of supernatant progesterone and estradiol by chemiluminescence, human placental lactogen （HPL） and human chorionic gonadotropin （ β - HCG） by radioimmtmoassay. Results MLN64 mRNA expression decreased by 26.91% in WT group as compared with N group, and increased in groups B and T by 69. 93%, 53.98%, respectively, when compared with WT group. The levels of estrogen and progesterone were 143 ± 19 pg/ml, 2. 42 ±1.43 ng/ml, respectively, in T group, and 110 ±22 pg/ml and 78 ±0.42 ng/ml, respectively, in WT group, the difference was significant （P 〈0. 05）. Conclusion Trophocyte saccharometabolism disorders, which can reduce MLN64 mRNA expression, may affect the rate -limiting steps of steroid hormone synthesis. Berberine and troglitazone, increasing MLN64 mRNA expression, are equal in effect. Except troglitazone, the other drugs have not significant effect on placental hormone secretion.