Improvement of Cerebral Ischemia-Reperfusion Injury via Regulation of Apoptosis by Exosomes Derived from BDNF-Overexpressing HEK293

Brain-derived neurotrophic factor (BDNF) provides neuroprotective effects towards therapeutic cerebral ischemia-reperfusion (I/R) injury. This view has been proposed by more and more evidence. However, due to the lack of permeability of the blood-brain barrier (BBB) as well as the brief half-life in...

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Bibliographic Details
Published in:BioMed research international 2021, Vol.2021, p.6613510-8
Main Authors: Wang, Lizong, Jiang, Jinghan, Zhou, Taofeng, Xue, Xiang, Cao, Yongjun
Format: Article
Language:English
Subjects:
Animals
Antibodies
Apoptosis
Blood-brain barrier
Brain damage
Brain Ischemia - metabolism
Brain Ischemia - therapy
Brain research
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - biosynthesis
Calcium
Calcium ions
Cardiovascular disease
Care and treatment
Cell Line, Tumor
Cell organelles
Cerebral ischemia
Control
Development and progression
Exosomes
Exosomes - metabolism
Exosomes - transplantation
Flow cytometry
Genetic aspects
Health aspects
HEK293 Cells
Humans
Hypoxia
Injury prevention
Ischemia
Membrane permeability
Membrane potential
Mitochondria
Nervous system
Neuroprotection
Oxidative stress
Proteins
Rats
Rats, Sprague-Dawley
Reperfusion
Reperfusion injury
Reperfusion Injury - metabolism
Reperfusion Injury - therapy
Stem cells
Stroke
Veins & arteries
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Summary:Brain-derived neurotrophic factor (BDNF) provides neuroprotective effects towards therapeutic cerebral ischemia-reperfusion (I/R) injury. This view has been proposed by more and more evidence. However, due to the lack of permeability of the blood-brain barrier (BBB) as well as the brief half-life in serum, clinical application is not widespread. To study the participation of exosomes containing BDNF in I/R, we isolated exosomes from BDNF-overexpressing HEK293. The protective outcomes of exosomes in hypoxia/reoxygenation (H/R) experiments were determined by the use of SY-5Y cells. Exosome-BDNF therapy restrained H/R-induced apoptosis by inhibition of the reducing levels of oxidative stress and calcium ions in the cells while maintaining stable levels of mitochondrial membrane potential in brain cells damaged by I/R. We then constructed a cerebral I/R injury model using SD rats to find the function of BDNF in exosome-mediated neuroprotection. The in vivo experiments conducted established that exosomes from BDNF-overexpressing HEK293 cells improved cerebral I/R injury by concealing neuronal apoptosis. Findings gained demonstrated that BDNF is a part of preventing cerebral I/R injury due to exosome mediation by regulating the cellular internal environment and inhibiting apoptosis.
ISSN:2314-6133
2314-6141
DOI:10.1155/2021/6613510