Objectives To investigate the relationship between the birth weight of fetus and the P~(70)S6K from ribosome in ceHs of placental tissues and investigate whether insulin can affect the P~(70)S6K by the P13 K/AKT/mTOR(P~(70)S6K)signaling pathway in the cells of the placental tissues and more regulate the birth weight of fetus. Methotis (1)60 cases of mature placental tissues after uterine-incision delivery without complications in the gestational period were selected as the investigated subiects.they were divided into three groups according to their birth welights. groupl. the weigh of the fetus≥4000 g,group2.3000 g≤the weisht of the fetus＜4000 g,group3.the weight of the fetus＜3000 g,(2)10 cases of mature placental tissues and 20 cases of villus in the early pregnant the fetus that were divided into insulin group.rapamycin group and control group according to stimulating factors. investigations on the insulin affection activities of P70s6K were carned out by immunoprecipitation, incoparation of[r-32P]ATP,tissue cell culture, Westem blotting. Results (1)P~(70)S6K activities in mature placental tissues(2546±357),(2333±318),(2111±315)cpm/mg,there were significant statistical differences in the comparison every two groups.(2)The P~(70)S6K activities in the placenta from the insulin stimulation group was significantly elevated. the P~(70)S6K activities in the placenta from the rapamycin stimulation group was significantly declined. there were statistical significance when each was compared with control group(P＜0.01).(3)P~(70)S6K activities in the nutrient cells of earlier pregnant period and protein expression will be elevated under insulin stimulating. However, that would be declined under rapamycin stimulating, it was statistical significant when each group compared with the control group(P＜0.01).Conclusion The activities of p~(70)S6K increased with the increase in the birth weight of the fetus, there was certain relationship between the activities of p~(70)S6K in the placental tissues and the birth weight of the fetus and Insulin can regulate the activities of P~(70)S6K in the placenta and earlier nutrient cells.%目的 探讨胎儿出生体重与胎盘组织细胞中p~(70)S6K关系及在胎盘组织细胞中胰岛素是否可通过磷酸肌醇三激酶/苏氨酸激酶/雷帕霉素靶蛋白(P~(70)S6激酶)[P13K/AKT/mTOR(p~(70)S6K)]信号通路调节p~(70)S6K,进而调节胎儿出生体重.方法 (1)60例足月无妊娠期合并症及并发症孕妇剖宫产后胎盘组织按胎儿出生体重分3组,1组:出生体重≥4000 g,2组:3000 g≤出生体重＜4000 g,3组:出生体重＜3000 g.(2)10例足月剖宫产后胎盘组织及20例早孕绒毛组织,按刺激因素分成3组,胰岛素组,雷帕霉素组及对照组,采用免疫沉淀、[r-32P]ATP掺入、组织细胞培养、Wester印迹技术对P~(70)S6K活性及胰岛素通过信号通路发挥作用的机制进行研究.结果 (1)在足月胎盘组织中p~(70)S6K活性分别为(2546±357)、(2333±318)及(2111±315)cpm/mg,1组＞2组＞3组,两两比较差异有统计学意义.(2)胰岛素作用足月胎盘组织细胞的P70S6K使其活性增强,mTOR特异性抑制剂雷帕霉素作用后p~(70)S6K活性下降,均与对照组比较,差异均有统计学意义(均P＜0.01).(3)胰岛素作用后使早孕滋养细胞p~(70)S6K活性增强及蛋白表达增加,雷帕霉素作用后使早孕滋养细胞p~(70)S6K活性及蛋白表达明显下降,均与对照组相比,差异均有统计学意义(均P＜0.01).结论 P~(70)S6K活性随出生体重增加而增加,因此在胎盘组织细胞中P~(70)S6K活性与胎儿出生体重相关,胰岛素可调节早孕滋养细胞及足月胎盘组织中P~(70)S6K.
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