分子营养 Molecular Nutrition

血红素铁对妊娠母鼠繁殖成绩及组织铁调基因表达的影响

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  • 云南农业大学动物科学技术学院, 云南省动物营养与饲料重点试验室, 昆明 650021
李美荃(1986-),女,黑龙江哈尔滨人,博士研究生,从事动物营养与饲料科学研究。E-mail:limeiquan2010@163.com

收稿日期: 2016-12-01

  网络出版日期: 2017-06-07

基金资助

云南省重大科技计划——生物育种(2012ZA018-3)

Effects of Heme Iron on Reproductive Performance and Iron-Regulated Gene Expressions in Tissues of Pregnant Mice

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  • Key Laboratory of Animal Nutrition and Feed Science of Yunnan Province, College of Animal Science and Technology, Yunnan Agricultural University, Kunming 650021, China

Received date: 2016-12-01

  Online published: 2017-06-07

摘要

本试验旨在探索血红素铁与硫酸亚铁(FeSO4)对妊娠母鼠繁殖成绩,妊娠母鼠组织与胎鼠铁含量,妊娠母鼠组织铁调素(hepcidin)、膜铁转运蛋白(Fpn)、猫白血病病毒C亚类受体(Flvcr)、转铁蛋白受体1(Tfr1)、转铁蛋白受体2(Tfr2)、二价金属转运体1(DMT1)和血红素转运蛋白(HCP)表达的影响。随机选取2月龄体况接近的昆明小鼠母鼠80只,随机分为8组,分别为对照组、缺铁组、血红素铁组(15、60、90 mg/kg血红素铁)、FeSO4组(75、300、450 mg/kg FeSO4),每组10只。配种受孕起对照组饲喂正常饲粮(基础饲粮中添加400 mg/kg FeSO4);其他各组均饲喂基础饲粮,妊娠第10~13天注射40 mg/kg去铁胺(DFO),诱导妊娠母鼠缺铁模型;妊娠第14天血红素铁组和FeSO4组开始在基础饲粮中添加血红素铁或FeSO4,缺铁组不添加。试验期为妊娠后1~20 d。结果表明:1)60 mg/kg血红素铁组胎鼠重最高,极显著高于对照组与缺铁组(P<0.01)。2)60 mg/kg血红素铁组与450 mg/kg FeSO4组母鼠血液血红蛋白(HGB)含量、红细胞数(RBC)和红细胞容积(HCT)极显著高于缺铁组(P<0.01)。3)60 mg/kg血红素铁组胎鼠铁含量最高,极显著高于对照组与FeSO4组(P<0.01);450 mg/kg FeSO4组母鼠肝脏、脾脏和胎盘铁含量均为最高。4)90 mg/kg血红素铁组和450 mg/kg FeSO4组母鼠肝脏hepcidin表达量较高,极显著高于缺铁组与对照组(P<0.01);15 mg/kg血红素铁组母鼠肝脏FpnTfr2表达量较高,极显著高于对照组和缺铁组(P<0.01);60 mg/kg血红素铁组母鼠肝脏Tfr1Flvcr表达量较高,极显著高于对照组和缺铁组(P<0.01);75 mg/kg FeSO4组母鼠肝脏Tfr1表达量较高,极显著高于对照组和缺铁组(P<0.01)。5)缺铁组母鼠十二指肠FpnHCPDMT1Flvcr表达量均极显著高于对照组(P<0.01)。6)缺铁组母鼠胎盘FpnTfr1DMT1FlvcrHCP表达量极显著高于对照组(P<0.01);90 mg/kg血红素铁组和450 mg/kg FeSO4组母鼠胎盘hepcidin表达量较高,极显著高于缺铁组与对照组(P<0.01)。7)饲粮血红素铁添加量为61.00 mg/kg或FeSO4添加量为336.11 mg/kg时,胎鼠铁含量最高;饲粮血红素铁添加量为93.49 mg/kg时,母鼠肝脏铁含量最高。综合得出,母鼠饲粮中添加适宜量的血红素铁或FeSO4均可显著促进胎鼠增重,诱导母鼠靶组织铁调基因的表达,提高母鼠组织和妊娠20 d胎鼠机体铁含量;HCPFlvcr在母鼠肠道对血红 素铁吸收或胎盘转运起至关重要的作用,但肠道吸收或胎盘转运FeSO4主要以DMT1Tfr2为主。

本文引用格式

李美荃, 张春勇, 计乔平, 陈克嶙, 郭荣富 . 血红素铁对妊娠母鼠繁殖成绩及组织铁调基因表达的影响[J]. 动物营养学报, 2017 , 29(6) : 1996 -2009 . DOI: 10.3969/j.issn.1006-267x.2017.06.021

Abstract

This study was conducted to compare the effects of heme iron (Fe) and ferrous sulfate (FeSO4) on reproductive performance, the Fe content in pregnant mice tissues and fetal mice, and the expressions of Fe-regulated genes[hepcidin, ferroportin (Fpn), feline leukemia virus subgroup C receptor (Flvcr), heme carrier protein (HCP), transferrin receptor 1 (Tfr1), transferrin receptor 2 (Tfr2) and divalent metal transporter 1 (DMT1)] in tissues of pregnant mice. Eighty Kunming female mice with similar body condition at 2 months of age were selected and randomly divided into 8 groups with 10 mice per group. The groups were control group, Fe deficiency group, heme Fe (15, 60 and 90 mg/kg) groups and FeSO4 (75, 300 and 450 mg/kg) groups. Since pregnant, control group was fed normal diet (a basal diet supplemented with 400 mg/kg FeSO4); the other groups were fed the basal diet, and were injected 40 mg/kg deferoxamine to induce Fe deficiency model at 10 to 13 d of pregnant; heme Fe and FeSO4 were supplemented in heme Fe groups and FeSO4 groups from 14 d of pregnant, while none of them was supplemented in Fe deficiency group. The experiment was carried out at 1 to 20 d of pregnant. The results showed as follows:1) the weight of fetal mice in 60 mg/kg group was significantly higher than that in control group and Fe deficiency group (P<0.01). 2) Blood hemoglobin (HGB) content, red blood cell (RBC) and hematocrit (HCT) in 60 mg/kg heme Fe group and 450 mg/kg FeSO4 group were significantly higher than those in Fe deficiency group (P<0.01). 3) The Fe content in the fetal mice in 60 mg/kg heme Fe group was significantly higher than that in control group and FeSO4 groups (P<0.01); the Fe content in liver, spleen and placenta was the highest in450 mg/kg FeSO4 group. 4) The expression of hepcidin in liver of pregnant mice was higher in 90 mg/kg heme Fe group and 450 mg/kg FeSO4 group, which was significantly higher than that in Fe deficiency group and control group (P<0.01); the expressions of Fpn and Tfr2 in liver in 15 mg/kg heme Fe group were higher, which were significantly higher than those in Fe deficiency group and control group (P<0.01); the expressions of Tfr1 and Flvcr in liver in 60 mg/kg heme Fe group were higher, which were significantly higher than those in Fe deficiency group and control group (P<0.01); the expression of Tfr1 in liver in 75 mg/kg FeSO4 group was higher, which was significantly higher than that in Fe deficiency group and control group (P<0.01). 5) Fpn, HCP, DMT1 and Flvcr expressions in duodenum of pregnant mice in Fe deficiency group were significantly higher than those in control group (P<0.01). 6) Placenta Fpn, HCP, DMT1, Flvcr and Tfr1 expressions were significantly higher than those in control group (P<0.01); the expression of hepcidin in placenta in 90 mg/kg heme Fe and 450 mg/kg FeSO4 was higher, which was significantly higher than that in Fe deficiency group and control group (P<0.01). 7) The Fe content of fetal mice was the highest when heme Fe was 61.00 mg/kg or FeSO4 was 336.11 mg/kg; the Fe content in liver of pregnant mice was the highest when heme Fe was 93.49 mg/kg. In conclusion, the supplementation of heme Fe and FeSO4 at proper levels can increase the weight of fetal mice, regulate the expressions of Fe-regulating genes in target tissues of pregnant mice, and increase the body Fe content of pregnancy mice and 20 d fetal mice; HCP and Flvcr play critical roles in the intestinal absorption or placental transport of heme Fe, while intestinal absorption and placental transport of FeSO4 mainly rely on DMT1 and Tfr2.

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