ArticleMolecular neurobiology2021
Preconditioning Exercise in Rats Attenuates Early Brain Injury Resulting from Subarachnoid Hemorrhage by Reducing Oxidative Stress, Inflammation, and Neuronal Apoptosis.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Exercise Improves Mitochondrial Homeostasis: A Potential Neuroprotective Strategy for Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2026Review
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
- iRhom2 deletion protects against diabetic neuropathy by suppressing neuroinflammation.The Journal of pharmacology and experimental therapeutics · 2026Article
- Non-Electrophilic Activation of NRF2 in Neurological Disorders: Therapeutic Promise of Non-Pharmacological Strategies.Antioxidants (Basel, Switzerland) · 2025Review
- Research progress of early brain Injury in subarachnoid hemorrhage from 2004 to 2024: a bibliometric analysis.Neurosurgical review · 2025Review
- Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K-AKT pathway by bioinformatic analysis.Experimental brain research · 2024Article
- Conditioning-based therapeutics for aneurysmal subarachnoid hemorrhage - A critical review.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Review
- Research hotspots and frontiers of preconditioning in cerebral ischemia: A bibliometric analysis.Heliyon · 2024Review
- Article
- Complications of COVID-19 on the Central Nervous System: Mechanisms and Potential Treatment for Easing Long COVID.Aging and disease · 2023Review
- Effects of different remote ischemia perconditioning methods on cerebral infarct volume and neurological impairment in rats.Scientific reports · 2023Article
- Andrographolide Attenuates Blood-Brain Barrier Disruption, Neuronal Apoptosis, and Oxidative Stress Through Activation of Nrf2/HO-1 Signaling Pathway in Subarachnoid Hemorrhage.Neurotoxicity research · 2022Article
- Pre-ischemic exercise prevents inflammation and apoptosis by inhibiting MAPK pathway in ischemic stroke.Translational neuroscience · 2022Article
- Insight Into the Mechanism of Exercise Preconditioning in Ischemic Stroke.Frontiers in pharmacology · 2022Review
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Subarachnoid hemorrhage (SAH) is a catastrophic form of stroke responsible for significant morbidity and mortality. Oxidative stress, inflammation, and neuronal apoptosis are important in the pathogenesis of early brain injury (EBI) following SAH. Preconditioning exercise confers neuroprotective effects, mitigating EBI; however, the basis for such protection is unknown. We investigated the effects of preconditioning exercise on brain damage and sensorimotor function after SAH. Male rats were assigned to either a sham-operated (Sham) group, exercise (Ex) group, or no-exercise (No-Ex) group. After a 3-week exercise program, they underwent SAH by endovascular perforation. Consciousness level, neurological score, and sensorimotor function were studied. The expression of nuclear factor erythroid 2 p45-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), 4-hydroxynonenal (4HNE), nitrotyrosine (NT), ionized calcium-binding adaptor molecule 1 (Iba1), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1β (IL-1β), 14-3-3γ, p-β-catenin Ser37, Bax, and caspase-3 were evaluated by immunohistochemistry or western blotting. The terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end labeling (TUNEL) assay was also performed. After SAH, the Ex group had significantly reduced neurological deficits, sensorimotor dysfunction, and consciousness disorder compared with the No-Ex group. Nrf2, HO-1, and 14-3-3γ were significantly higher in the Ex group, while 4HNE, NT, Iba1, TNF-α, IL-6, IL-1β, Bax, caspase-3, and TUNEL-positive cells were significantly lower. Our findings suggest that preconditioning exercise ameliorates EBI after SAH. The expression of 4HNE and NT was reduced by Nrf2/HO-1 pathway activation; additionally, both oxidative stress and inflammation were reduced. Furthermore, preconditioning exercise reduced apoptosis, likely via the 14-3-3γ/p-β-catenin Ser37/Bax/caspase-3 pathway.
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