Downregulation of Lgals3 Alleviates Inflammatory Response and Apoptosis in a Mouse Model of Cerebral Ischemia/Reperfusion Injury.
Overview
- Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Department of Rehabilitation Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
- School of Basic Medicine, Nanjing Medical University, Nanjing, China
Abstract
Purpose: The present work investigated the expression and function of Lgals3 in cerebral ischemia/
Methods: Differentially expressed genes in cerebral IR were analyzed by the Gene Expression Omnibus (GEO) microarray. A middle cerebral artery occlusion (MCAO) mouse model was constructed. Adeno‐associated virus serotype 9 vector carrying Lgals3 shRNA was administered to mice via tail vein injection. Four weeks after virus administration, mice were subjected to MCAO modeling. Neurological function was reflected by evaluating the neurological deficit score. To assess infarct size and neuronal apoptosis, triphenyl tetrazolium chloride (TTC) staining and TUNEL assay were performed. The concentrations of IL‐6, TNF‐α, IL‐4, and IL‐1β in brain tissues were measured using enzyme‐linked immunosorbent assay (ELISA). Co‐immunoprecipitation (Co‐IP) was performed to examine the interaction between Lgals3 and TLR4. In addition, real‐time quantitative reverse transcription‐polymerase
Results: GEO bioinformatics analysis revealed that Lgals3 expression was significantly upregulated in cerebral IR. MCAO mouse model was successfully established, and Lgals3 was markedly upregulated in brain tissues of MCAO mice. Lgals3 knockdown reduced infarct volume, improved neurological deficit scores, and inhibited neuronal apoptosis, accompanied by decreased levels of pro‐inflammatory cytokines (IL‐6, TNF‐α, and IL‐1β) and increased levels of anti‐inflammatory cytokine IL‐4 in brain tissues of MCAO mice. Lgals3 silencing inhibited the activation of the TLR4/
Conclusion: Lgals3 knockdown alleviates neuroinflammation and neuronal apoptosis in brain tissues of mice with cerebral IR injury. The present findings indicate that Lgals3 participates in the progression of cerebral IR injury, and may serve as a potential intervention target for ameliorating cerebral IR damage.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE97537 — at NCBI GEO; found in “Data Availability Statement”
Other data links
- ncbi.nlm.nih.gov/
geo — NCBI; found in the text, “Microarray‐Based Gene Expression Analysis…”
Data Availability Statement
The datasets generated and/
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 7 authors, 4 keywords, 16 MeSH terms, 37 references.
Cite
This paper
Gan, Z., Lai, H., Yang, Y., Lu, J., Zhang, W., Xiao, J., & Xu, G. (2026). Downregulation of Lgals3 Alleviates Inflammatory Response and Apoptosis in a Mouse Model of Cerebral Ischemia/
BibTeX
@article{gan2026downregu
author = {Gan, Zhaodan and Lai, Haifang and Yang, Yun and Lu, Jun and Zhang, Wen and Xiao, Jianqiu and Xu, Guangxu},
title = {{Downregulation of Lgals3 Alleviates Inflammatory Response and Apoptosis in a Mouse Model of Cerebral Ischemia/
journal = {Brain and behavior},
year = {2026},
month = aug,
volume = {16},
number = {8},
pages = {e71700},
publisher = {Wiley},
issn = {2162-3279},
doi = {10.1002/
url = {https://
pmid = {42625424},
pmcid = {PMC13494508}
}
RIS
TY - JOUR
AU - Gan, Zhaodan
AU - Lai, Haifang
AU - Yang, Yun
AU - Lu, Jun
AU - Zhang, Wen
AU - Xiao, Jianqiu
AU - Xu, Guangxu
TI - Downregulation of Lgals3 Alleviates Inflammatory Response and Apoptosis in a Mouse Model of Cerebral Ischemia/
T2 - Brain and behavior
J2 - Brain Behav
PY - 2026
DA - 2026/
VL - 16
IS - 8
SP - e71700
SN - 2162-3279
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1002/
"type": "article-journal",
"title": "Downregulation of Lgals3 Alleviates Inflammatory Response and Apoptosis in a Mouse Model of Cerebral Ischemia/
"container-title": "Brain and behavior",
"author": [
{
"family": "Gan",
"given": "Zhaodan"
},
{
"family": "Lai",
"given": "Haifang"
},
{
"family": "Yang",
"given": "Yun"
},
{
"family": "Lu",
"given": "Jun"
},
{
"family": "Zhang",
"given": "Wen"
},
{
"family": "Xiao",
"given": "Jianqiu"
},
{
"family": "Xu",
"given": "Guangxu"
}
],
"container-title-short":
"volume": "16",
"issue": "8",
"page": "e71700",
"DOI": "10.1002/
"PMID": "42625424",
"PMCID": "PMC13494508",
"ISSN": "2162-3279",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
8,
1
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1155/humu/4033506
- SELL Marks an Effector-Deficient CD8&
lt;sup& gt;+& lt;/ sup& gt; T Cell Subset That Promotes Intracerebral Hemorrhage and Responds to Rutin Therapy. Journal: Human mutationIn common: stroke, mouse, 2 references - [2] doi:10.1016/j.isci.2026.115779
- Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/
NLRP3 pathway. Journal: iScienceIn common: stroke, mouse, cellular / molecular, 1 reference - [3] doi:10.1016/j.neurot.2026.e00977
- Exosome-mediated delivery of 3-n-butylphthalide rescues microglial energy crisis and ameliorates neuroinflammation in ischemic stroke.Journal: Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeuticsIn common: stroke, mouse, cellular / molecular, 1 reference
- [4] doi:10.1186/s12929-026-01271-w
- Lack of cortistatin drives neuroimmune and vascular dysfunction in brain ischemia.Journal: Journal of biomedical scienceIn common: stroke, mouse, cellular / molecular, 1 reference
- [5] doi:10.1186/s12974-026-03794-3
- Single-cell omics and flow cytometry identify distinct immune states of dural and brain-infiltrating IL-17-producing γδ T cells after experimental stroke.Journal: Journal of neuroinflammationIn common: stroke, mouse, cellular / molecular, 1 reference
- [6] doi:10.1007/s10565-026-10177-0
- Multi-omics analysis and experimental validation reveal the IRF7-CXCL10 axis as a master regulator of microglial PCD in ischemic stroke.Journal: Cell biology and toxicologyIn common: stroke, mouse, cellular / molecular, 1 reference
- [7] doi:10.1016/j.xpro.2026.104716
- Protocol for studying Chemerin 15-enhanced microglial phagocytosis in cerebral ischemia-reperfusion injury via the ChemR23/
p38 MAPK pathway. Journal: STAR protocolsIn common: stroke, cellular / molecular, 1 reference - [8] doi:10.1016/j.isci.2026.117108 [code]
- PVT inhibition mitigates neuropathology and cognitive deficits in chronic cerebral hypoperfusion.Journal: iScienceIn common: stroke, 1 reference
- [9] doi:10.3389/fnins.2026.1881087
- Dual-graph attention autoencoder for spatial domain identification in ischemic stroke.Journal: Frontiers in neuroscienceIn common: stroke, 1 reference
- [10] doi:10.1186/s13062-026-00912-2
- Integrated analysis of single-cell transcriptome identifies a glial-neurovascular signaling trajectory in brain repair after ischemia.Journal: Biology directIn common: stroke, mouse, cellular / molecular
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.