ArticleCell transplantation2019
Initiating TrkB/Akt Signaling Cascade Preserves Blood-Brain Barrier after Subarachnoid Hemorrhage in Rats.
Article in Cell transplantation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- GPR30 Inhibits Neuronal Apoptosis After Subarachnoid Hemorrhage by Activating the Wnt/β-Catenin Pathway in a m6A-dependent Manner.Molecular neurobiology · 2025Article
- Mechanisms and potential therapeutic molecular targets in blood-brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury.Frontiers in neurology · 2025Review
- N-acetylserotonin Derivative Exerts a Neuroprotective Effect by Inhibiting the NLRP3 Inflammasome and Activating the PI3K/Akt/Nrf2 Pathway in the Model of Hypoxic-Ischemic Brain Damage.Neurochemical research · 2021Article
- Underlying Mechanisms and Potential Therapeutic Molecular Targets in Blood-Brain Barrier Disruption after Subarachnoid Hemorrhage.Current neuropharmacology · 2020Review
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
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Abstract
The integrity of the blood-brain barrier (BBB) plays a vital role in affecting the prognosis of subarachnoid hemorrhage (SAH). This study aimed to investigate activation of the Tropomyosin-related kinase receptor B (TrkB) and its downstream signaling pathway on preserving BBB breakdown after experimental SAH. An endovascular perforation SAH model was applied. N-[2-(5-hydroxy-1H-indol-3-yl) ethyl]-2- oxopiperidine-3-carboxamide (HIOC), the derivative of N-acetyl serotonin (NAS), was intracerebroventricularly administered 3 h after SAH induction. The neurologic scores and brain water content were evaluated in an outcome study. Western blot and immunofluorescence staining were used to investigate the mechanism. The results indicated that HIOC activated the TrkB/Akt pathway, increased the tight junction expression, improved neurologic deficits, and ameliorated brain edema after SAH. Thus, we conclude that initiating the TrkB/Akt signaling cascade preserves BBB breakdown after experimental SAH in rats.
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