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[1]郭碧云,林昊,陳琴.鐵調(diào)素緩解間歇性低氧誘導(dǎo)的心肌細胞鐵沉積[J].福建醫(yī)藥雜志,2025,47(02):55-60.[doi:10.20148/j.fmj.2025.02.015]
 GUO Biyun,LIN Hao,CHEN Qin.Hepcidin alleviates intermittent hypoxia-induced iron deposition in cardiomyocytes[J].FUJIAN MEDICAL JOURNAL,2025,47(02):55-60.[doi:10.20148/j.fmj.2025.02.015]
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鐵調(diào)素緩解間歇性低氧誘導(dǎo)的心肌細胞鐵沉積()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
47
期數(shù):
2025年02期
頁碼:
55-60
欄目:
基礎(chǔ)研究
出版日期:
2025-02-20

文章信息/Info

Title:
Hepcidin alleviates intermittent hypoxia-induced iron deposition in cardiomyocytes
文章編號:
1002-2600(2025)02-0055-06
作者:
郭碧云12林昊2陳琴345
1 福建醫(yī)科大學(xué)附屬福州市第一總醫(yī)院綜合重癥醫(yī)學(xué)科,福州 350004; 2 福建醫(yī)科大學(xué)附屬協(xié)和醫(yī)院急診科,福州 350001; 3 福建醫(yī)科大學(xué)附屬協(xié)和醫(yī)院心內(nèi)科,福州 350001; 4 福建省心血管病醫(yī)學(xué)中心,福州 350001; 5 福建省冠心病研究所,福州 350001
Author(s):
GUO Biyun12 LIN Hao2 CHEN Qin345
1 Department of Integrated Intensive Care Medicine,Fuzhou First General Hospital Affiliated to Fujian Medical University,Fuzhou,Fujian 350004,China; 2 Department of Emergency,Fujian Medical University Union Hospital,Fuzhou,Fujian 350001,China; 3 Department of Cardiology,Fujian Medical University Union Hospital,Fuzhou,Fujian 350001,China; 4 Fujian Heart Medical Center,Fuzhou,Fujian 350001,China; 5 Fujian Institute of Coronary Heart Disease,Fuzhou,Fujian 350001,China
關(guān)鍵詞:
Hamp mRNA 鐵調(diào)素 間歇性低氧 鐵轉(zhuǎn)運蛋白1
Keywords:
Hamp mRNA Hepcidin intermittent hypoxia FPN1
分類號:
R445
DOI:
10.20148/j.fmj.2025.02.015
文獻標(biāo)志碼:
A
摘要:
目的 本研究旨在探討鐵調(diào)素(Hepcidin)是否可以通過調(diào)節(jié)鐵代謝,減輕對間歇性低氧(intermittent hypoxia,IH)誘導(dǎo)的小鼠心肌細胞的損傷。方法 間歇性低氧培養(yǎng)HL-1心肌細胞并轉(zhuǎn)染Hamp過表達質(zhì)粒,檢測細胞內(nèi)Hamp mRNA、Hepcidin蛋白水平; 觀察細胞生存情況; 觀察細胞內(nèi)活性鐵及總活性氧(ROS)水平; 檢測細胞內(nèi)缺氧誘導(dǎo)因子-1α(HIF-1α)及調(diào)節(jié)鐵代謝關(guān)鍵蛋白(FPN1、FBXL5和IRPs)的表達水平。結(jié)果 鐵調(diào)素通過下調(diào)鐵轉(zhuǎn)運蛋白1(FPN1)的表達(P<0.01),顯示出降低暴露于間歇性低氧的HL-1細胞中Fe2+和ROS水平的能力(P<0.05); 此外,鐵調(diào)素介導(dǎo)HIF-1α和IRPs的表達(P<0.05),這些蛋白可能參與鐵相關(guān)轉(zhuǎn)運蛋白的調(diào)節(jié)。結(jié)論 鐵調(diào)素可以在一定程度上減輕低氧刺激誘導(dǎo)的心肌鐵沉積和ROS損傷。
Abstract:
Objective The aim of this study was to investigate whether Hepcidin can reduce the injury of mouse cardiomyocytes induced by intermittent hypoxia by regulating iron metabolism. Methods HL-1 cardiomyocytes were cultured with intermittent hypoxia and transfected with Hamp overexpression plasmid.Hamp mRNA and Hepcidin protein levels were detected.The survival of cells was observed.The levels of labile iron and total ROS that induced iron death were observed.The expression levels of HIF-1α and key proteins regulating iron metabolism(FPN1, FBXL5 and IRPs)were detected.Results Hepcidin down-regulates the expression of ferritransporter 1(FPN1)protein(P<0.01), and shows the ability to reduce Fe2+ and ROS levels in HL-1 cells exposed to intermittent hypoxia(P<0.05).In addition, Hepcidin mediates HIF-1α and IRPs(P<0.01).These proteins may be involved in the regulation of iron-related transporters.Conclusion Hepcidin can alleviate myocardial iron deposition and ROS injury induced by hypoxia stimulation to a certain extent.

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備注/Memo

備注/Memo:
基金項目:福建省自然科學(xué)基金(2021J01752)
通信作者:陳 琴,Email:[email protected]
更新日期/Last Update: 2025-02-20