Allicin promotes functional recovery in ischemic stroke via glutathione peroxidase-1 activation of Src-Akt-Erk

Allicin exhibits various pharmacological activities and has been suggested to be beneficial in the treatment of stroke. However, the underlying mechanisms are largely unknown. Here, we confirmed that allicin protected the brain from cerebral injury, which could be ascribed to its anti‑apoptotic and...

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Bibliographic Details
Published in:Cell death discovery 2023-09, Vol.9 (1), p.335-335, Article 335
Main Authors: Zhuang, Fei, Shi, Xin, Qiao, Sen, Liu, Bin, Wang, Zhimei, Huo, Huanhuan, Liang, Feng, Shen, Linghong, Zhu, Lijuan, He, Ben, Wang, Hongmei
Format: Article
Language:English
Subjects:
631/378/2596/1308
631/378/340
AKT protein
Apoptosis
Arachidonic acid
Astrocytes
Biochemistry
Biomedical and Life Sciences
Brain injury
Cell Biology
Cell Cycle Analysis
Cerebral infarction
Extracellular signal-regulated kinase
Glutathione peroxidase
Homeostasis
Hypoxia
Inflammation
Ischemia
Kinases
Life Sciences
Lipid metabolism
Lipid peroxidation
Lipids
Metabolomics
Phosphorylation
Proteomics
Recovery of function
Src protein
Stem Cells
Stroke
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Summary:Allicin exhibits various pharmacological activities and has been suggested to be beneficial in the treatment of stroke. However, the underlying mechanisms are largely unknown. Here, we confirmed that allicin protected the brain from cerebral injury, which could be ascribed to its anti‑apoptotic and anti‑inflammatory effects, as well as the regulation of lipid metabolism, using proteomics and metabolomics analysis. Our results suggested that allicin could significantly ameliorate behavioral characteristics, cerebral infarct area, cell apoptosis, inflammatory factors, and lipid metabolic-related factors (arachidonic acid, 15-hydroperoxy-eicosatetraenoic acid (15S-HPETE), palmitoylcarnitine, and acylcarnitine) by recalibrating astrocyte homeostasis in mice with photothrombotic stroke (PT). In astrocytes, allicin significantly increased glutathione peroxidase 1 (GPX1) levels and inhibited the arachidonic acid-related pathway, which was also observed in the brains of mice with PT. Allicin was proven to inhibit hypoxia-induced astrocyte apoptosis by increasing GPX1 expression, activating proto-oncogene tyrosine-protein kinase Src (Src)- protein kinase B (AKT)-extracellular signal-regulated kinase (ERK) phosphorylation, and decreasing lipid peroxidation. Thus, we concluded that allicin significantly prevented and ameliorated ischemic stroke by increasing GPX1 levels to complete the complex physiological process.
ISSN:2058-7716
2058-7716
DOI:10.1038/s41420-023-01633-5