• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

[铁过载小鼠模型的建立及其对骨髓造血的影响]

[Establishment of an mouse model of iron-overload and its impact on bone marrow hematopoiesis].

作者信息

Chai Xiao, Zhao Ming-feng, Li De-guan, Meng Juan-xia, Lu Wen-yi, Mu Juan, Meng Ai-min

机构信息

Department of Hematology, Tianjin First Central Hospital, the First Central Clinical College of Tianjin Medical University, Tianjin 300192, China.

出版信息

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2013 Oct;35(5):547-52. doi: 10.3881/j.issn.1000-503X.2013.05.012.

DOI:10.3881/j.issn.1000-503X.2013.05.012
PMID:24183045
Abstract

OBJECTIVE

To establish a mouse model of iron overload by intraperitoneal injection of iron dextran and investigate the impact of iron overload on bone marrow hematopoiesis.

METHODS

A total of 40 C57BL/6 mice were divided into control group, low-dose iron group (12.5 mg/ml), middle-dose iron group (25 mg/ml), and high-dose iron group (50 mg/ml). The control group received normal saline (0.2 ml), and the rest were injected with intraperitoneal iron dextran every three days for six weeks. Iron overload was confirmed by observing the bone marrow, hepatic, and splenic iron deposits and the bone marrow labile iron pool. In addition, peripheral blood and bone marrow mononuclear cells were counted and the hematopoietic function was assessed.

RESULTS

Iron deposits in bone marrow, liver, and spleen were markedly increased in the mouse models. Bone marrow iron was deposited mostly within the matrix with no significant difference in expression of labile iron pool.Compared with control group, the ability of hematopoietic colony-forming in three interventional groups were decreased significantly (P<0.05). Bone marrow mononuclear cells counts showed no significant difference. The amounts of peripheral blood cells (white blood cells, red blood cells, platelets, and hemoglobin) in different iron groups showed no significant difference among these groups;although the platelets were decreased slightly in low-dose iron group [(780.7±39.60)×10(9)/L], middle dose iron group [(676.2±21.43)×10(9)/L], and high-dose iron group [(587.3±19.67)×10(9)/L] when compared with the control group [(926.0±28.23)×10(9)/L], there was no significant difference(P>0.05).

CONCLUSIONS

The iron-overloaded mouse model was successfully established by intraperitoneal administration of iron dextran. Iron overload can damage the hepatic, splenic, and bone marrow hematopoietic function, although no significant difference was observed in peripheral blood count.

摘要

目的

通过腹腔注射右旋糖酐铁建立铁过载小鼠模型,并研究铁过载对骨髓造血的影响。

方法

将40只C57BL/6小鼠分为对照组、低剂量铁组(12.5 mg/ml)、中剂量铁组(25 mg/ml)和高剂量铁组(50 mg/ml)。对照组给予生理盐水(0.2 ml),其余组每三天腹腔注射一次右旋糖酐铁,共六周。通过观察骨髓、肝脏和脾脏的铁沉积以及骨髓不稳定铁池来确认铁过载。此外,对外周血和骨髓单个核细胞进行计数,并评估造血功能。

结果

小鼠模型中骨髓、肝脏和脾脏的铁沉积明显增加。骨髓铁主要沉积在基质内,不稳定铁池的表达无显著差异。与对照组相比,三个干预组的造血集落形成能力显著降低(P<0.05)。骨髓单个核细胞计数无显著差异。不同铁组外周血细胞(白细胞、红细胞、血小板和血红蛋白)数量在各组间无显著差异;虽然低剂量铁组[(780.7±39.60)×10⁹/L]、中剂量铁组[(676.2±21.43)×10⁹/L]和高剂量铁组[(587.3±19.67)×10⁹/L]的血小板数量与对照组[(926.0±28.23)×10⁹/L]相比略有下降,但差异无统计学意义(P>0.05)。

结论

通过腹腔注射右旋糖酐铁成功建立了铁过载小鼠模型。铁过载可损害肝脏、脾脏和骨髓的造血功能,尽管外周血细胞计数未观察到显著差异。

相似文献

1
[Establishment of an mouse model of iron-overload and its impact on bone marrow hematopoiesis].[铁过载小鼠模型的建立及其对骨髓造血的影响]
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2013 Oct;35(5):547-52. doi: 10.3881/j.issn.1000-503X.2013.05.012.
2
[Effects and mechanism of iron overload on hematopoiesis in mice with bone marrow injury].[铁过载对骨髓损伤小鼠造血功能的影响及机制]
Zhonghua Xue Ye Xue Za Zhi. 2014 Nov;35(11):1000-4. doi: 10.3760/cma.j.issn.0253-2727.2014.11.011.
3
The bone marrow hematopoietic microenvironment is impaired in iron-overloaded mice.铁过载小鼠的骨髓造血微环境受损。
Eur J Haematol. 2014 Aug;93(2):118-28. doi: 10.1111/ejh.12309. Epub 2014 Mar 28.
4
[Establishment and Identification of MDS Mouse Model with Irom Overload].[铁过载骨髓增生异常综合征小鼠模型的建立与鉴定]
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2018 Aug;26(4):1129-1136. doi: 10.7534/j.issn.1009-2137.2018.04.031.
5
[Effects of oxidative stress on hematopoiesis of hematopoietic stem and progenitor cells with iron overload].[氧化应激对铁过载状态下造血干细胞和祖细胞造血作用的影响]
Zhonghua Yi Xue Za Zhi. 2011 Dec 13;91(46):3284-8.
6
[Establishment of iron overloaded bone marrow model in vitro and its impact on hematopoiesis].[体外铁过载骨髓模型的建立及其对造血的影响]
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2011 Aug;19(4):1038-42.
7
[Impacts of iron overload on hematopoiesis and its microenvironment].[铁过载对造血及其微环境的影响]
Rinsho Ketsueki. 2015 Jun;56(6):577-85. doi: 10.11406/rinketsu.56.577.
8
Protective effects of deferasirox and N-acetyl-L-cysteine on iron overload-injured bone marrow.地拉罗司和N-乙酰半胱氨酸对铁过载损伤骨髓的保护作用。
Braz J Med Biol Res. 2017 Oct 19;50(12):e6087. doi: 10.1590/1414-431X20176087.
9
[Establishment of an Iron-overloaded Mouse Model with Tuberculosis and Analysis of the Iron Metabolism Index].[建立铁过载合并肺结核小鼠模型及铁代谢指标分析]
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2021 Jun 30;43(3):357-365. doi: 10.3881/j.issn.1000-503X.13336.
10
Establishment of secondary iron overloaded mouse model: evaluation of cardiac function and analysis according to iron concentration.继发性铁过载小鼠模型的建立:根据铁浓度评估心脏功能并进行分析。
Pediatr Cardiol. 2011 Oct;32(7):947-52. doi: 10.1007/s00246-011-0019-4. Epub 2011 Jun 9.

引用本文的文献

1
Role of reactive oxygen species in myelodysplastic syndromes.活性氧在骨髓增生异常综合征中的作用。
Cell Mol Biol Lett. 2024 Apr 14;29(1):53. doi: 10.1186/s11658-024-00570-0.
2
[Effect of cyclophosphamide on hematopoietic stem cells in mice with iron overload].[环磷酰胺对铁过载小鼠造血干细胞的影响]
Nan Fang Yi Ke Da Xue Xue Bao. 2020 Jan 30;40(1):110-117. doi: 10.12122/j.issn.1673-4254.2020.01.18.
3
[Effects of iron overload on the peripheral blood T cells in mice].[铁过载对小鼠外周血T细胞的影响]
Zhonghua Xue Ye Xue Za Zhi. 2016 Jun 14;37(6):535-7. doi: 10.3760/cma.j.issn.0253-2727.2016.06.021.