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Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage

Background: Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3 (Gal-3) is one of the scaffold proteins of Galectins. Studies have indicated that Gal-3 plays an important role in the physi...

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Autores principales: Liang, Tianyu, Zhu, Zheng, Gong, Fangxiao, Yang, Xiaobo, Lei, Xiaoju, Lu, Ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10522396/
https://www.ncbi.nlm.nih.gov/pubmed/37698533
http://dx.doi.org/10.18632/aging.205014
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author Liang, Tianyu
Zhu, Zheng
Gong, Fangxiao
Yang, Xiaobo
Lei, Xiaoju
Lu, Ling
author_facet Liang, Tianyu
Zhu, Zheng
Gong, Fangxiao
Yang, Xiaobo
Lei, Xiaoju
Lu, Ling
author_sort Liang, Tianyu
collection PubMed
description Background: Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3 (Gal-3) is one of the scaffold proteins of Galectins. Studies have indicated that Gal-3 plays an important role in the physiological and pathological state of the nervous system. Here we focus on the role of Gal-3 in ICH, especially in neuroinflammation. Methods: Injection of autologous blood into the right basal ganglia was used to simulate ICH injury, and the level of Gal-3 in brain was regulated by related means. The changes of Gal-3 were detected by western blot and immunofluorescence, the level of neuroinflammation by immunofluorescence staining and ELISA. Apoptosis and neuron loss were detected by TUNEL staining FJB staining and Nissl staining, and neurological deficits were judged by neurobehavioral tests. Results: The protein level of Gal-3 increased at 24 h after ICH. Downregulation of Gal-3 level can reduce the infiltration of M1-type microglia and peripheral inflammatory cells, thus alleviating post-ICH neuroinflammation, and reducing cell apoptosis and neuron loss in brain tissue. ICH-induced neurological damage was rescued. Meanwhile, the promotion in the expression level of Gal-3 increased neuroinflammatory activation and nerve cell death, aggravating ICH-induced brain injury. Conclusions: This study proves that Gal-3 is involved in neuroinflammation and nerve damage after ICH. Gal-3 expression should not be encouraged early on to prevent neuroinflammation. which provides a new possibility for clinical treatment for ICH patients.
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spelling pubmed-105223962023-09-27 Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage Liang, Tianyu Zhu, Zheng Gong, Fangxiao Yang, Xiaobo Lei, Xiaoju Lu, Ling Aging (Albany NY) Research Paper Background: Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3 (Gal-3) is one of the scaffold proteins of Galectins. Studies have indicated that Gal-3 plays an important role in the physiological and pathological state of the nervous system. Here we focus on the role of Gal-3 in ICH, especially in neuroinflammation. Methods: Injection of autologous blood into the right basal ganglia was used to simulate ICH injury, and the level of Gal-3 in brain was regulated by related means. The changes of Gal-3 were detected by western blot and immunofluorescence, the level of neuroinflammation by immunofluorescence staining and ELISA. Apoptosis and neuron loss were detected by TUNEL staining FJB staining and Nissl staining, and neurological deficits were judged by neurobehavioral tests. Results: The protein level of Gal-3 increased at 24 h after ICH. Downregulation of Gal-3 level can reduce the infiltration of M1-type microglia and peripheral inflammatory cells, thus alleviating post-ICH neuroinflammation, and reducing cell apoptosis and neuron loss in brain tissue. ICH-induced neurological damage was rescued. Meanwhile, the promotion in the expression level of Gal-3 increased neuroinflammatory activation and nerve cell death, aggravating ICH-induced brain injury. Conclusions: This study proves that Gal-3 is involved in neuroinflammation and nerve damage after ICH. Gal-3 expression should not be encouraged early on to prevent neuroinflammation. which provides a new possibility for clinical treatment for ICH patients. Impact Journals 2023-09-11 /pmc/articles/PMC10522396/ /pubmed/37698533 http://dx.doi.org/10.18632/aging.205014 Text en Copyright: © 2023 Liang et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Liang, Tianyu
Zhu, Zheng
Gong, Fangxiao
Yang, Xiaobo
Lei, Xiaoju
Lu, Ling
Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage
title Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage
title_full Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage
title_fullStr Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage
title_full_unstemmed Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage
title_short Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage
title_sort galectin-3 promotes brain injury by modulating the phenotype of microglia via binding tlr-4 after intracerebral hemorrhage
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10522396/
https://www.ncbi.nlm.nih.gov/pubmed/37698533
http://dx.doi.org/10.18632/aging.205014
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