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机构地区:[1]华中科技大学同济医学院附属同济医院中西医结合研究所,武汉430030
出 处:《中华围产医学杂志》2003年第3期160-163,共4页Chinese Journal of Perinatal Medicine
基 金:国家自然科学基金资助 (3 9870 92 3 )
摘 要:目的 探讨葡萄糖转运蛋白 (GL UT)的表达在胎儿生长受限 (fetal growth restriction,FGR)发生发展中的作用以及补肾益气活血防治 FGR的分子机制。 方法 用被动吸烟法建立 FGR大鼠的动物模型 ,并分为正常对照组、FGR组、FGR中药治疗组 (中药组 )和 FGR左旋精氨酸治疗组(L- Arg组 ) ,利用 RT- PCR和 Western blot的方法分别检测各组孕鼠胎盘葡萄糖转运蛋白 (GL U T)家族中 GL U T1 、GL UT3的 m RNA含量和蛋白浓度 ,同时还观察胎鼠和母鼠血清葡萄糖水平。 结果 FGR胎鼠血清葡萄糖 (2 .7± 0 .9) mm ol/ L 较正常组 (5 .3± 1.5 ) m mol/ L 明显降低 (P<0 .0 1) ;胎鼠血清葡萄糖在正常组及中药组之间以及各组母体血清葡萄糖之间都无明显差异 (P>0 .0 5 ) ;FGR组胎盘中 GL UT1 和 GL U T3的 m RNA含量及蛋白浓度较正常组明显降低 ,经补肾益气活血方治疗 ,孕鼠胎盘中两者的含量同正常组比较无明显差异。 结论 GL U T1 和 GL UT3参与了 FGR的病理生理过程 ;补肾益气活血方通过增强 GL U T1 和 GL U T3的基因的表达 ,提高胎鼠血清葡萄糖水平来防治 FGR。Objective To explore the effect of glucose transporter(GLUT) on the course of fetal growth restriction(FGR) and molecular mechanism of Chinese herbal medicine(CHM) on supplementing kidney and Qi, and activating blood circulation in treating FGR. Methods The rat FGR model was established by passive smoking. Forty cases were divided into four groups, i.e. normal control group, CHM treating group, FGR group and L-Arg treating group.The mRNA and protein levels of GLUT 1 and GLUT 3 in pregnant rats' placenta were detected by RT-PCR and Western-blot respectively, serum glucose in maternal and fetal blood were detected as well. Results Serum glucose level in FGR group is significantly lower than that of control group (2.7±0.9) mmol/L vs (5.3 ±1.5) mmol/L P <0.01. There is no statistical difference between CHM group and control group(4.5±1.5) mmol/L vs (5.3±1.5) mm/L( P >0.05). No difference is found among three groups (6.2 ±1.2) mmol/L vs (5.5±1.5) mmol/L vs (6.3±1.6) mmol/L ( P >0.05). The decrease of GLUT 1 mRNA and GLUT 3 mRNA could be detected in FGR rats and no difference be detected between control group and CHM group ( P >0.05) ;similar changes in protein level were observed. Conclusions GLUT 1 and GlUT 3 play an important role in occurrence and development of FGR, It is a possible mechanism for CHM to treat FGR by enhancing expression and transcription of GLUT 1 and GLUT 3.
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