Candesartan Reduces Neuronal Apoptosis Caused by Ischemic Stroke via Regulating the FFAR1/ITGA4 Pathway

Ischemic stroke (IS) is a general term for necrosis of brain tissue caused by stenosis, occlusion of arteries supplying blood to the brain (carotid artery and vertebral artery), and insufficient blood supply to the brain. Cerebral ischemia is the main kind of IS causing cell damage. However, the und...

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Published in:Mediators of inflammation 2022-09, Vol.2022, p.1-14
Main Authors: Ding, Yubao, Lang, Yue, Zhang, Hui, Li, Yu, Liu, Xiao, Li, Minjie
Format: Article
Language:English
Subjects:
Antibodies
Apoptosis
Candesartan
Carotid artery
Caspase-3
Cell viability
Cerebral blood flow
Cluster analysis
Fatty acids
Flow cytometry
Gene expression
Genes
Ischemia
Ligands
Neurons
Pheochromocytoma cells
Plasmids
Proteins
Reagents
Software
Statistical analysis
Stenosis
Stroke
Stroke (Disease)
Trends
Vertebrae
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creator Ding, Yubao
Lang, Yue
Zhang, Hui
Li, Yu
Liu, Xiao
Li, Minjie
description Ischemic stroke (IS) is a general term for necrosis of brain tissue caused by stenosis, occlusion of arteries supplying blood to the brain (carotid artery and vertebral artery), and insufficient blood supply to the brain. Cerebral ischemia is the main kind of IS causing cell damage. However, the underlying mechanism still needs to be clarified further. In this study, it was demonstrated that FFAR1 was a hub gene in IS. The expression of FFAR1 was increased in PC12 cells with OGD/R treatment. FFAR1 deficiency inhibited cell viability and induced cell apoptosis, which was reversed by FFAR1 overexpression. Moreover, candesartan, as a compound targeting FFAR1, facilitated cell viability and reduced cell apoptosis. The expression of ITGA4 was also high in OGD/R-PC12 cells as FFAR1. Furthermore, FFAR1 deficiency retarded the increasing of cell viability and inhibition of cell apoptosis by downregulation of Bax and Cleaved Caspase-3 in OGD/R-PC12 cells with candesartan treatment. In conclusion, candesartan may regulate neuronal apoptosis through FFAR1/ITGA4 axis.
doi_str_mv 10.1155/2022/2356507
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Cerebral ischemia is the main kind of IS causing cell damage. However, the underlying mechanism still needs to be clarified further. In this study, it was demonstrated that FFAR1 was a hub gene in IS. The expression of FFAR1 was increased in PC12 cells with OGD/R treatment. FFAR1 deficiency inhibited cell viability and induced cell apoptosis, which was reversed by FFAR1 overexpression. Moreover, candesartan, as a compound targeting FFAR1, facilitated cell viability and reduced cell apoptosis. The expression of ITGA4 was also high in OGD/R-PC12 cells as FFAR1. Furthermore, FFAR1 deficiency retarded the increasing of cell viability and inhibition of cell apoptosis by downregulation of Bax and Cleaved Caspase-3 in OGD/R-PC12 cells with candesartan treatment. 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subjects Antibodies
Apoptosis
Candesartan
Carotid artery
Caspase-3
Cell viability
Cerebral blood flow
Cluster analysis
Fatty acids
Flow cytometry
Gene expression
Genes
Ischemia
Ligands
Neurons
Pheochromocytoma cells
Plasmids
Proteins
Reagents
Software
Statistical analysis
Stenosis
Stroke
Stroke (Disease)
Trends
Vertebrae
title Candesartan Reduces Neuronal Apoptosis Caused by Ischemic Stroke via Regulating the FFAR1/ITGA4 Pathway
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