ArticleInternational journal of molecular medicine2019
Hyperforin improves post-stroke social isolation‑induced exaggeration of PSD and PSA via TGF-β.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Decreased hippocampal neurogenesis and post-stroke depression.Frontiers in psychiatry · 2026Review
- Advancing Post-Stroke Depression Research: Insights from Murine Models and Behavioral Analyses.Life (Basel, Switzerland) · 2024Review
- Hyperforin ameliorates neuroinflammation and white matter lesions by regulating microglial VEGFRCNS neuroscience & therapeutics · 2024Article
- Exploring the Potential Molecular Mechanism of the Shugan Jieyu Capsule in the Treatment of Depression through Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation.Current computer-aided drug design · 2024Article
- Reversal of the detrimental effects of social isolation on ischemic cerebral injury and stroke-associated pneumonia by inhibiting small intestinalJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Neutrophil Heterogeneity and its Roles in the Inflammatory Network after Ischemic Stroke.Current neuropharmacology · 2023Article
- Possible Engagement of Nicotinic Acetylcholine Receptors in Pathophysiology of Brain Ischemia-Induced Cognitive Impairment.Journal of molecular neuroscience : MN · 2022Review
- proBDNF expression induces apoptosis and inhibits synaptic regeneration by regulating the RhoA-JNK pathway in an in vitro post-stroke depression model.Translational psychiatry · 2021Article
- (Biological psychiatry global open science · 2021Article
- Improving Cognition with Nutraceuticals Targeting TGF-β1 Signaling.Antioxidants (Basel, Switzerland) · 2021Review
- Understanding Why Post-Stroke Depression May Be the Norm Rather Than the Exception: The Anatomical and Neuroinflammatory Correlates of Post-Stroke Depression.Journal of clinical medicine · 2021Review
- Canonical transient receptor potential channels and their modulators: biology, pharmacology and therapeutic potentials.Archives of pharmacal research · 2021Review
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke survivors often experience social isolation, which can lead to post‑stroke depression (PSD) and post‑stroke anxiety (PSA) that can compromise neurogenesis and impede functional recovery following the stroke. The present study aimed to investigate the effects and mechanisms of post‑stroke social isolation‑mediated PSD and PSA on hippocampal neurogenesis and cognitive function. The effects of the natural antidepressant hyperforin on post‑stroke social isolation‑mediated PSD and PSA were also investigated. In the present study, a model of PSD and PSA using C57BL/6J male mice was successfully established using middle cerebral artery occlusion combined with post‑stroke isolated housing conditions. It was observed that PSD and PSA were more prominent in the isolated mice compared with the pair‑housed mice at 14 days post‑ischemia (dpi). Mice isolated 3 dpi exhibited decreased transforming growth factor‑β (TGF‑β) levels and impairment of hippocampal neurogenesis and memory function at 14 dpi. Intracerebroventricular administration of recombinant TGF‑β for 7 consecutive days, starting at 7 dpi, restored the reduced hippocampal neurogenesis and memory function induced by social isolation. Furthermore, intranasal administration of hyperforin for 7 consecutive days starting at 7 dpi improved PSD and PSA and promoted hippocampal neurogenesis and memory function in the isolated mice at 14 dpi. The inhibition of TGF‑β with a neutralizing antibody prevented the effects of hyperforin. In conclusion, the results revealed a previously uncharacterized role of hyperforin in improving post‑stroke social isolation‑induced exaggeration of PSD and PSA and, in turn, promoting hippocampal neurogenesis and cognitive function via TGF‑β.
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Registered trials
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