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在6-羟基多巴胺诱导的帕金森病大鼠模型中,铁蓄积和小胶质细胞激活导致黑质高回声。

Iron accumulation and microglia activation contribute to substantia nigra hyperechogenicity in the 6-OHDA-induced rat model of Parkinson's disease.

作者信息

Zhu Yaqin, Wang Bao, Tao Kai, Yang Hengli, Wang Yixiao, Zhou Tian, Yang Yilin, Yuan Lijun, Liu Xi, Duan Yunyou

机构信息

Department of Ultrasound, Tangdu Hospital of the Fourth Military Medicine University, Xi'an 710038, China.

Institute for Functional Neurosurgery of PLA, Department of Neurosurgery, Tangdu Hospital of the Fourth Military Medicine University, Xi'an 710038, China.

出版信息

Parkinsonism Relat Disord. 2017 Mar;36:76-82. doi: 10.1016/j.parkreldis.2017.01.003. Epub 2017 Jan 6.

DOI:10.1016/j.parkreldis.2017.01.003
PMID:28108264
Abstract

INTRODUCTION

This study aims to explain the mechanisms for the formation of sonographic features of Parkinson's disease (PD) using a 6-hydroxydopamine (6-OHDA) rat model of PD. The iron chelator deferiprone (DFP) was used in the PD model rat to examine the relationship between iron and the echo signal.

METHODS

Rat models were created using stereotactic injections of 6-OHDA. DFP was administered intragastrically. Transcranial sonography (TCS) was performed to observe the substantia nigra (SN) echo signal of the brain. Immunofluorescence and iron staining were performed to observe the histological characteristics of the hyperechogenic area. The imaging findings were compared with the histopathological findings.

RESULTS

The PD model rat presented a large area of hyperechogenicity in the SN. Ferric ion accumulation and microglia proliferation occurred in the hyperechogenic area. DFP inhibited dopaminergic (DA) neuron necrosis, ferric ion accumulation and microglia proliferation and reduced the hyperechogenic area of the SN.

CONCLUSIONS

Both iron aggregation and gliosis contribute to the formation of substantia nigra hyperechogenicity (SNH) in PD. DFP exhibits a neuroprotective effect by inhibiting SNH. Iron deposit and the SNH are correlated with DA neuron necrosis.

摘要

引言

本研究旨在利用帕金森病(PD)的6-羟基多巴胺(6-OHDA)大鼠模型解释PD超声特征的形成机制。在PD模型大鼠中使用铁螯合剂去铁酮(DFP)来研究铁与回声信号之间的关系。

方法

通过立体定向注射6-OHDA建立大鼠模型。DFP经胃内给药。进行经颅超声检查(TCS)以观察脑黑质(SN)的回声信号。进行免疫荧光和铁染色以观察高回声区的组织学特征。将影像学结果与组织病理学结果进行比较。

结果

PD模型大鼠的SN出现大面积高回声。高回声区出现铁离子积聚和小胶质细胞增殖。DFP抑制多巴胺能(DA)神经元坏死、铁离子积聚和小胶质细胞增殖,并减少SN的高回声区。

结论

铁聚集和胶质增生均有助于PD中黑质高回声(SNH)的形成。DFP通过抑制SNH发挥神经保护作用。铁沉积和SNH与DA神经元坏死相关。

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