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Lnc-FOXD3-AS1通过激活SMAD1/5/8促进缺铁性贫血大鼠体内Hepcidin表达

安媛媛·安林 籍雁敏 热西丹·阿布力海提 木尼热·买买提尼牙孜 佐日汗·艾依萨

河北医学2023,Vol.29Issue(12):1992-1998,7.
河北医学2023,Vol.29Issue(12):1992-1998,7.DOI:10.3969/j.issn.1006-6233.2023.12.011

Lnc-FOXD3-AS1通过激活SMAD1/5/8促进缺铁性贫血大鼠体内Hepcidin表达

Lnc-FOXD3-AS1 Promotes the Expression of Ferrimodulin in Rats with Iron Deficiency Anemia by Activating SMAD1/5/8

安媛媛·安林 1籍雁敏 1热西丹·阿布力海提 2木尼热·买买提尼牙孜 2佐日汗·艾依萨1

作者信息

  • 1. 新疆医科大学第七附属医院儿科, 新疆 乌鲁木齐 830000
  • 2. 新疆医科大学第二附属医院儿科, 新疆 乌鲁木齐 830000
  • 折叠

摘要

Abstract

Objective:To investigate the regulatory effect of long-chain noncoding RNA FOXD3-AS1(Lnc-FoxD3-AS1)on the expression of hepcidin in rats with iron deficiency anemia(IDA).Methods:The IDA model was induced by repeated bloodletting and feeding low iron diet to SD rats without specific pathogen grade.The rats were divided into control group,IDA group,IDA rats treated with LCN-FoxD3-AS1 overex-pression group(pcDNA-FOXD3-AS1+IDA group),IDA rats treated with empty vector expression group(pcDNA-null+IDA group),and IDA rats treated with pcDNA-FOXD3-AS1 combined with Sm ad1/5/8 acti-vation inhibitor Compound C treatment group(pcDNA-FOXD3-AS1+Compound C+IDA group),n=8 for each group.The content of iron in blood of rats in each group was detected by kit method,the expression of Lnc-FOXD3-AS1 in liver tissue and serum was detected by qRT-PCR,and the expression and activation of ferrimodulin and SMAD1/5/8 protein in liver tissue and serum were detected by western blot and ELISA.Re-sults:Iron deficiency anemia model was successfully induced in IDA group.Compared with the control group,iron content in liver tissue and serum of rats in IDA group remained in the state of iron deficiency(all P<0.05),and the expression levels of ferrimodulin,LCNC-FOXD3-AS1 and SMAD1/5/8 were significantly de-creased(all P<0.05),and the phosphorylation level of SMAD1/5/8 was significantly decreased(all P<0.05).Compared with pcDNA-null+IDA group,iron content in liver tissue and serum in pcDNA-FOXD3-AS1 +IDA group was significantly increased(all P<0.05),and the expression levels of ferrimodulin,LCNA-FOXD3-AS1 and SMAD1/5/8 were significantly increased(all P<0.05).Moreover,the phosphorylation lev-el of SMAD1/5/8 was significantly increased(P<0.05).Compared with pcDNA-FOXD3-AS1+IDA group,the iron content in liver tissue and serum of pcDNA-FOXD3-AS1+Compound C+IDA group was significantly decreased(all P<0.05),and the expression levels of ferromodulin and SMAD1/5/8 were significantly de-creased(all P<0.05).Conclusion:lnc-FOXD3-AS1 is downregulated in the IDA rat model,and it pro-motes the expression of Hepcidin by activating the SMAD1/5/8 pathway.This study is of great significance for a deeper understanding of the biological network mechanisms underlying IDA occurrence.

关键词

长链非编码RNA FOXD3-AS1/SMAD1/5/8/缺铁性贫血大鼠模型/Hepcidin

Key words

Long non-coding RNA FOXD3-AS1/Smad 1/5/8/Iron deficiency anemia rat mod-el/Hepcidin

引用本文复制引用

安媛媛·安林,籍雁敏,热西丹·阿布力海提,木尼热·买买提尼牙孜,佐日汗·艾依萨..Lnc-FOXD3-AS1通过激活SMAD1/5/8促进缺铁性贫血大鼠体内Hepcidin表达[J].河北医学,2023,29(12):1992-1998,7.

基金项目

新疆少数民族科技人才特殊培养计划科研项目,(编号:2020D03007) (编号:2020D03007)

河北医学

OACSTPCD

1006-6233

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