Expression and role of peroxiredoxin 1 in rats after intracerebral hemorrhage

Objective To investigate the cellular localization of peroxiredoxin 1 (Prdx1) in the central nervous system, and its expression changes and possible mechanisms after intracerebral hemorrhage (ICH). Methods Five 8~10-week old SD rats underwent cerebral perfusion, and the brain tissue was sectioned fo...

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Main Authors: YANG Guoqiang, HUANG Jiacheng, YUAN Junjie, ZHANG Qin, GONG Changxiong, XIE Lexing, XIONG Xiaoyi, YANG Qingwu
Format: Article
Language:zho
Published: Editorial Office of Journal of Third Military Medical University 2020-02-01
Series:Di-san junyi daxue xuebao
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Online Access:http://aammt.tmmu.edu.cn/Upload/rhtml/201909060.htm
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Summary:Objective To investigate the cellular localization of peroxiredoxin 1 (Prdx1) in the central nervous system, and its expression changes and possible mechanisms after intracerebral hemorrhage (ICH). Methods Five 8~10-week old SD rats underwent cerebral perfusion, and the brain tissue was sectioned for immunofluorescence staining to observe the localization of Prdx1 in the neurons, astrocytes and microglia. A total of 35 SD rats were randomly divided into sham group, and ICH for 12 h, and 1, 2, 3, 4 and 5 d groups (n=5). The ICH model was established by autologous blood injection in the latter 5 groups, and the sham group was treated with the same amount of normal saline as the control. The expression of Prdx1 at mRNA and protein levels in each group was detected by qRT-PCR and Western blotting. Prdx1 interference plasmid or blank vector were transfected into HeLa cells, and RNA-seq was performed to detect the differentially expressed genes (DEGs) in 2 groups of cells. GO analysis was performed on DEGs to predict the possible role of Prdx1 in ICH. Results Immunofluorescence staining showed that Prdx1 was mainly distributed in the NeuN+ neurons in the cortex, while in the striatum, Prdx1 was mainly in the astrocytes. Western blot and qRT-PCR results showed that Prdx1 significantly increased on the 3rd day after ICH (P < 0.05), and gradually decreased with elapse of time. RNA-seq and Go analysis suggested that the DEGs caused by Prdx1 were mainly involved in the inflammatory response, apoptosis, innate immune response, axon development and other pathways associated with secondary injury of ICH. Conclusion Prdx1 has different distribution characteristics in different cerebral regions. After ICH, Prdx1 is significantly elevated, and it may be associated with inflammation, immune response, and axon development in ICH.
ISSN:1000-5404