ArticleExperimental and therapeutic medicine2020
Dl-3n-butylphthalide improves spatial learning and memory in rats with vascular dementia by reducing autophagy via regulation of the mTOR signaling pathway.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- EGb761 suppressed vascular dementia via modulating Wnt/β-catenin signaling pathway-induced apoptosis and autophagy in hippocampal neuronal cells.European journal of medical research · 2025Article
- mTOR signaling and Alzheimer's disease: What we know and where we are?CNS neuroscience & therapeutics · 2024Review
- Bloodletting Acupuncture at Jing-Well Points on Hand Induced Autophagy to Alleviate Brain Injury in Acute Altitude Hypoxic Rats by Activating PINK1/Parkin Pathway.Chinese journal of integrative medicine · 2023Article
- DL-3-N-Butylphthalide Promotes Cartilage Extracellular Matrix Synthesis and Inhibits Osteoarthritis Development by Regulating FoxO3a.Oxidative medicine and cellular longevity · 2022Article
- Neuroplasticity to autophagy cross-talk in a therapeutic effect of physical exercises and irisin in ADHD.Frontiers in molecular neuroscience · 2022Review
- Review
- Pharmacological Treatment of Vascular Dementia: A Molecular Mechanism Perspective.Aging and disease · 2021Review
- Therapeutic Potential of Remote Ischemic Conditioning in Vascular Cognitive Impairment.Frontiers in cellular neuroscience · 2021Review
- Efficacy and safety of butylphthalide as adjunctive therapy for vascular dementia: A protocol for systematic review and meta-analysis.Medicine · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dl-3n-butylphthalide (NBP) has been reported to be a beneficial and promising drug for the treatment and prevention of vascular dementia (VD). NBP has been demonstrated to improve learning and memory in rats with vascular cognitive impairment by activating the silent information regulator 1/brain-derived neurotrophic factor pathway. However, NBP is a multi-target drug. Therefore, the present study aimed to determine whether the protective effects of NBP on learning deficits in a rat model of VD were due to the inhibition of autophagy via the phosphorylated mammalian target of rapamycin (p-mTOR) pathway. NBP treatment attenuated memory damage in rats with VD, as demonstrated by T-maze and Morris water maze tests. NBP administration also significantly reduced the levels of the characteristic autophagic proteins Beclin 1 and LC3II and upregulated phosphorylation levels of mTOR at Ser-2448 compared with the VD group. However, treatment of rats with VD with NBP plus the mTOR inhibitor rapamycin failed to significantly suppress Beclin 1 and LC3II expression. These results suggested that the beneficial effects of NBP on learning deficits in a rat model of VD were due to the suppression of ischemia-induced autophagy via the p-mTOR signaling pathway.
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