孕晚期母亲铁状态对胎盘ferroportin1表达的影响

目的研究孕晚期母亲不同铁营养状态下胎盘ferroportin1(FP1)的蛋白定位、蛋白表达及其mRNA的表达。方法临床选择不同铁营养状态的孕妇,收集分娩时的胎盘。采用免疫组织化学方法测定FP1蛋白的定位,Western Blot测定蛋白表达量的变化,采用实时定量RT-PCR测定mRNA表达。结果FP1蛋白主要表达在人足月胎盘的合体滋养细胞(STB)胞浆;母亲不同铁营养状态下胎盘FP1蛋白和mRNA的表达均无明显变化。结论孕晚期胎盘FP1蛋白和mRNA的表达不受孕妇铁状态的影响。     

镉暴露对母体钙代谢及胎盘钙转运的影响

钙代谢紊乱是镉毒性的重要方面[1]。妊娠状态下 ,母体钙代谢会发生一系列改变以满足胎儿的钙需求。在目前中国孕妇膳食钙摄入普遍不足的情况下 ,镉暴露对母体钙代谢会产生何种影响自然引起人们关注。另外 ,母体镉暴露是否影响胎盘钙转运也是一个值得探讨的问题。1　镉在母体、胎盘和胎儿的蓄积有研究表明 ,妊娠状态下镉在体内的蓄积较非妊娠时高。Bhatacharyya等[2 ]给小鼠经饮水低剂量 (0 11nmol/L)染镉 17d ,孕鼠肝、肾、十二指肠的镉蓄积分别是同龄非孕鼠的 2 6、2 8和4 7倍。黄思齐等[3 ]发现镉在母体主要蓄积在肝脏和肾脏 ,胎盘虽…     

胎盘铁转运的分子机制研究进展

铁从母体向胎儿的转运过程至今并不完全清楚.铁经过胎盘向胎儿的转运首先由位于胎盘滋养细胞母体面转铁蛋白受体1的吸收,然后来自母体的转铁蛋白再返回到母体血循环中.遗传性血色素沉着病缺陷蛋白可能参与了转铁蛋白受体1对转铁蛋白铁吸收的调节.滋养细胞顶端的铁蛋白受体也可能参与了胎盘的部分铁吸收.吸收入内吞小体里的铁很可能通过二价金属离子转运蛋白1转入胞浆.进入胞浆后.铁或以铁蛋白的形式贮存、或参与生物合成、或被转出滋养细胞,具体机制尚不清楚.铁转出滋养细胞很可能是通过位于其基底膜的膜铁转运蛋白1,但似乎还存在其它的转出路径.另外,参与胎盘输出铁氧化的铜氧化酶可能与膜铁转运辅助蛋白和血浆铜蓝蛋白都不同,且目前研究定位也不清楚.至于在滋养细胞基底面发现的转铁蛋白受体1、金属离子转运蛋白1、铁蛋白和遗传性血色素沉着病缺陷蛋白等是否参与胎盘铁的输出目前尚无支持的证据.因此,对于胎盘铁转运过程的理解还有许多工作要做.     

妊娠期糖尿病孕妇血脂变化与胎盘脂质转运

正常妊娠时,为了满足胎儿生长发育需要,妊娠期脂代谢将发生巨大变化。这些变化包括早、中孕期脂肪生成增加,晚孕期脂肪分解增加,主要表现为甘油三酯(TG)升高,磷脂和胆固醇也轻度升高。妊娠期糖尿病(GDM)孕妇因胰岛素抵抗(IR),抑制脂肪氧化和分解作用减弱,血脂较正常妊娠更高,并且TG水平与新生儿体重呈正相关。胎盘不能直接转运脂蛋白,TG需水解成脂肪酸才能通过胎盘。胎盘中脂肪酸转运蛋白(FATPs)、胎盘膜脂肪酸结合蛋白(pFABPpm)、脂蛋白脂酶(LPL)和内皮脂肪酶(EL)在脂肪酸转运中起重要作用,GDM孕妇通过增强其表达而影响胎儿生长发育。     

胎盘葡萄糖转运蛋白与胎儿生长受限

葡萄糖是哺乳类动物主要的能量来源,葡萄糖转运蛋白是细胞转运葡萄糖的载体,胎盘葡萄糖转运蛋白承担了妊娠期母儿间的葡萄糖转运,对满足胎儿生长发育的能量需求极为重要.对胎盘葡萄糖转运蛋白表达的研究,有助于进一步阐明胎儿生长受限的发生机制,并为其预防和治疗提供新的思路.     

肿瘤坏死因子-α、胎盘生长因子与妊高征的关系

肿瘤坏死因子在妊娠免疫与胎儿生长发育中发挥重要作用 ,含量增高时可引起滋养细胞和内皮功能损伤 ;胎盘生长因子属于血管内皮生长因子家族 ,促进早孕时滋养细胞增殖与分化 ,保证胎盘血管网络的充分形成 ,表达降低则可影响胎儿血供。该因子表达异常可能与妊高征时滋养细胞功能低下、血管内皮损伤有关 ,可能参与了妊高征的发生与发展     

胎盘组织白血病抑制因子和hCG的表达与妊娠期高血压疾病的关系

目的:探讨白血病抑制因子(LIF)基因和人绒毛膜促性腺激素(hCG)基因在胎盘组织的表达与妊娠期高血压疾病(HDCP)的关系。方法:采用荧光定量RT-PCR(FQ-RT-PCR)技术,对37例子痫前期患者、50例妊娠期高血压患者和80例正常足月妊娠妇女胎盘组织进行LIF-mRNA和hCG mRNA的检测,分析目的基因与β-actin拷贝数的比值。结果:①子痫前期组LIF mRNA的表达较妊娠期高血压组和正常对照组明显降低,差异有统计学意义(P0.01),且随着病情的加重,LIF mRNA表达下降。妊娠期高血压组和正常对照组比较,LIF mRNA的表达稍有降低,但差异无统计学意义(P0.05)。②hCG mRNA的表达水平均按照正常对照组、妊娠期高血压组、子痫前期组依次升高,子痫前期组与妊娠期高血压组、正常对照组比较差异有统计学意义(P0.01)。妊娠期高血压组与正常对照组比较,hCG mRNA表达水平的差异无统计学意义(P0.05)。③通过pearson相关分析,子痫前期组LIF mRNA的表达量和hCG mRNA的表达量相关系数为-0.57,呈显著性负相关(P0.05)。结论:HDCP患者胎盘中LIF表达下降和hCG水平升高,可能通过影响细胞滋养细胞的浸润能力而影响血管床的发育,共同参与了子痫前期的发病过程。     

高脂日粮对孕鼠胎盘养分转运及胎鼠宫内生长的影响

目的研究孕鼠妊娠期采食高脂日粮对胎盘养分转运、胎鼠宫内生长、胎鼠肝脏能量和甲基化代谢相关基因表达量的影响。方法母鼠妊娠后分别采食高脂和低脂日粮,妊娠20d收集母体血清、胎盘、胎鼠肝脏。检测母体血清代谢底物和瘦素浓度,通过RT-PCR方法检测胎盘葡萄糖和氨基酸转运载体的表达量,胎盘信号传导与转录活化因子-3(STAT3),以及胎鼠肝脏甲基转移酶和能量代谢相关基因的mRNA表达量。结果孕鼠采食高脂肪日粮显著提高胎鼠宫内生长速度,血清甘油三酯和瘦素浓度,且显著上调胎盘STAT3、葡萄糖转运载体Slc38a2的mRNA表达量。高脂日粮使胎鼠肝脏甲基转移酶DNMT1基因表达量上调,而使DNMT3a的基因表达量下调,并使胎鼠肝脏过氧化物酶增殖子激活受体γ(PPARγ)、糖皮质激素受体(GR)、Na-K-ATP酶(Na-K-ATP)mRNA表达量有提高趋势。结论孕鼠采食高脂日粮可能通过瘦素-STAT3途径上调养分转运载体的表达量促进胎鼠的宫内生长,胎鼠宫内生长加快会导致肝脏能量代谢和DNA甲基化相关基因表达量发生改变。     

Cord serum and placental tissue iron status in maternal hypoferremia.

Studies on 85 mothers with term infants and 32 mothers with preterm infants revealed that the cord serum and placental tissue iron levels were significantly reduced (P less than 0.001) in the mothers with hypoferremia (serum iron less than or equal to 50 microgram/100 ml). These levels were found to have linear correlations with the maternal serum iron levels, suggesting that the fetus and the placenta extracted iron in amounts proportional to the levels available in the mother. The high serum iron values in cord blood compared to the maternal blood even in the mothers with hypoferremia suggested that the process of active transfer of iron from mother to the fetus was maintained in maternal iron deficiency.     

The relationship between iron status and thyroid hormone concentration in iron-deficient adolescent Iranian girls

Extensive data from animal and human studies indicate that iron deficiency impairs thyroid metabolism. The aim of this study was to determine thyroid hormone status in iron-deficient adolescent girls. By stepwise random sampling from among all public high schools for girls in Lar and its vicinity in southern Iran, 103 out of 431 iron deficient subjects were selected. Urine and serum samples were collected and assayed for urinary iodine and serum ferritin, iron, total iron binding capacity (TIBC), thyroid stimulating hormone (TSH), thyroxine (T4), triiodothyronine (T3), free thyroid hormones (fT4 and fT3), triiodothyronine resin uptake (T3RU), reverse triiodothyronine (rT3), selenium and albumin concentrations. Hematological indices for iron status confirmed that all subjects were iron-deficient. There was a significant correlation between T4 and ferritin (r = 0.52, P < 0.001) and between TSH and ferritin (r = -0.3, P < 0.05). Subjects with low serum ferritin had a higher ratio of T3/T4 (r = -0.42, P < 0.01). Using stepwise regression analysis, only ferritin contributed significantly to the rT3 concentration (r = -0.35, P < 0.01). The results indicate that the degree of iron deficiency may affect thyroid hormone status in iron-deficient adolescent girls.     

Iron supplementation during infancy--effects on expression of iron transporters, iron absorption, and iron utilization in rat pups

BACKGROUND: Studies conducted in human infants suggest developmental changes in the regulation of iron absorption; however, little is known about the molecular mechanisms regulating iron absorption during infancy. Two intestinal iron transporters, divalent metal transporter 1 (DMT1) and ferroportin 1 (FPN1), were recently identified. OBJECTIVE: The objective was to investigate at a molecular level the regulation of iron absorption during infancy in a rat pup model. We examined the developmental expression of DMT1 and FPN1 and the effects of iron supplementation on their expression and on iron absorption and utilization during infancy. DESIGN: Rat pups were given daily oral doses of 0, 30, or 150 microg Fe from day 2 to day 20 after birth. On days 10 and 20 after birth, (59)Fe absorption, tissue minerals, and intestinal DMT1, FPN1, and ferritin expression were examined. To assess developmental expression, DMT1 and FPN1 were examined in control rats from days 1 to 50 after birth. RESULTS: Intestinal DMT1 and FPN1 were significantly affected by age; expression increased dramatically by day 40. On day 10, no significant effect of iron supplementation on DMT1 and FPN1 gene expression or on iron absorption was observed. By day 20, DMT1 and FPN1 expression and iron absorption had decreased significantly with iron supplementation. CONCLUSIONS: During early infancy, rat pups are unable to down-regulate intestinal iron transporters or iron absorption in response to iron supplementation, whereas down-regulation occurs during late infancy. The current findings provide evidence of the developmental regulation of iron absorption, which emphasizes the need for caution when giving iron supplements to infants at an early age.     

妊娠期并发症与胎盘细胞衰老相关性研究

胎盘随着孕龄增加而逐步老化是正常生理表现,但有一些胎盘会出现早衰。近来有研究报道,不良妊娠与胎盘异常衰老有关,包括胎膜早破、胎儿宫内死亡、子痫前期、胎盘植入等。本文对胎盘细胞衰老的特点及其与妊娠期并发症相关性的研究进行综述。     

镉暴露与大鼠胎盘屏障关系研究

目的探讨镉暴露能否通过SD大鼠胎盘屏障。方法雌性SD大鼠12只随机分为3组,每组4只,依次皮下注射去离子水(对照组)、20μg/kg体质量112Cd2+溶液(低剂量组)和40μg/kg体质量112Cd2+溶液(高剂量组),1次/d,连续注射52～55 d,其间在第31天开始与雄性SD大鼠按常规方法交配,孕第20天剖杀母鼠。取母鼠血、脐带血用原子吸收光谱仪测镉水平;用电感耦合等离子体质谱仪测胎鼠脑、肾脏、肝脏和胎盘镉水平。结果低剂量组和高剂量组的胎盘[(2.431±0.311)、(4.954±0.120)mg/kg]、脐血[(1.188±0.419)、(3.143±0.662)μg/L]和肝脏[(0.037±0.003)、(0.084±0.009)mg/kg]镉水平与对照组[(0.002±0.001)mg/kg、(0.114±0.018)μg/L、(0.010±0.003)mg/kg]比较,差异均有统计学意义(P<0.05);低、高剂量组胎鼠脑镉水平与对照组比较,差异无统计学意义(P>0.05)。结论镉可通过胎盘屏障到达胎鼠体内,并在胎盘蓄积。     

IL-6与支原体胎盘炎关系的研究

目的:观察支原体宫颈炎孕妇血清中IL-6水平变化,应用产后胎盘病理检查结果进行验证,求证IL-6对支原体胎盘炎的诊断价值。方法:将受试者分成宫颈支原体阴性组(正常孕妇组)、宫颈支原体阳性组。对两组孕妇血清IL-6水平进行定量检查,分别计算其平均值;对两组孕妇做产后胎盘病理检验,分别计算胎盘绒毛膜羊膜炎的发生率;对宫颈支原体阳性组做产后胎膜支原体培养,计算支原体感染胎盘炎的发生率。结果:宫颈支原体阳性组胎盘绒毛膜羊膜炎的发生率为37.25%,宫颈支原体阴性组为41.54%,两组差异无统计学意义(P>0.05),宫颈支原体阳性组中孕妇胎盘出现绒毛膜羊膜炎,胎膜支原体培养阳性,其血清IL-6明显升高,两组比较有统计学差异(P<0.05)。结论:孕妇血清中IL-6检测可以预测支原体胎盘炎。     

胎盘生长因子与急性冠状动脉综合征关系的研究

目的 探讨血清胎盘生长因子(PLGF)在急性冠状动脉综合征(ACS)临床诊断策略中的意义.方法 112例行冠状动脉造影患者根据临床资料和造影结果分为非冠心病(non-CAD)组27例、稳定型心绞痛(SA)组28例、不稳定型心绞痛(UA)组29例、急性心肌梗死(AMI)组28例.其中57例ACS患者按冠状动脉造影结果分为单支病变组19例、双支病变组16例、三支病变组22例,并根据Jenkins积分分为0～7分组23例、8～ 15分组27例、16～32分组7例.分别检测各组入院时血清PLGF水平,并进行比较.40例患者接受经皮冠状动脉介入治疗(PCI),分别检测术前30min、术后第1天、术后第2天血清PLGF水平.结果 AMI组血清PLGF水平为(38.33±10.14)ng/L,UA组血清PLGF水平为(37.44±13.32) ng/L,均显著高于SA组的(20.90±3.88) ng/L及non-CAD组的(20.34±4.53) ng/L(P＜ 0.01);AMI组与UA组、SA组与non-CAD组血清PLGF水平比较差异无统计学意义(P＞0.05).三支病变组、双支病变组、单支病变组血清PLGF水平两两比较差异均无统计学意义(P＞ 0.05);Jenkins积分0～7分组、8～ 15分组、16～32分组血清PLGF水平两两比较差异均无统计学意义(P＞0.05).40例接受PCI的患者术后第1天血清PLGF水平为(32.03±7.41) ng/L,显著高于术前的( 23.86±6.91) ng/L(P＜ 0.05),术后第2天血清PLGF水平[(29.37±6.99) ng/L]较术后第1天呈回落趋势(P＞0.05).经Pearson相关分析,AMI患者血清PLGF水平与心肌肌钙蛋白T及肌酸激酶同工酶-MB水平无显著相关性(r=-0.158,P=0.421;r=0.302,P=0.118).结论 血清PLGF水平是反映ACS患者冠状动脉粥样硬化斑块失稳定或斑块破裂的一个炎性标志物,对ACS疑似病例的早期诊断有一定的参考价值.     

晚期孕妇铁、锌、铜营养状况与贫血的关系

目的：了解晚期孕妇血清铁、锌、铜营养状况和缺铁性贫血的关系。方法：对在1999年12月-2000年2月期间来福建省福清市医院和妇幼保健院门诊检查的242名晚期孕妇采取空腹静脉血10ml，测定血红蛋白（Hb）、红细胞压积（Hct）和血清铁（Fe）、锌（Zn）、铜（Cu）、铁蛋白（SF）、可溶性转铁蛋白受体（s-TfR）的含量，同时测量身高、体重等指标。结果：贫血孕妇的血清Fe、Cu、SF含量显低于非贫血孕妇，而血清锌、s-TfR含量两组差异无显性。结论：孕妇贫血不仅与缺铁有关，同时伴有铜等微量元素的缺乏。     

The relationship between anthropometric measurements and measurements of iron status and susceptibility to malaria in Gambian children.

Anthropometric measurements were made and serum iron and ferritin levels determined in a group of Gambian children at the beginning of the rainy season and these findings were related to the malaria experience of the children during the following malaria transmission season. Susceptibility to malaria was not correlated with prior weight-for-age, height-for-age, weight-for-height or serum albumin, or with serum iron, serum iron binding capacity nor serum ferritin. Thus, our findings do not provide any support for the view that poor nutritional status, as assessed by anthropometric measurements, or iron deficiency protect against malaria infection. Children who developed a clinical attack of malaria accompanied by a high level of parasitaemia tended to have a higher mean weight-for-age at the beginning of the rainy season than did children who had a clinical attack accompanied by a low level of parasitaemia, but the difference between groups was not statistically significant. However, they had a significantly higher mean serum ferritin level (P less than 0.01).