ArticleInternational journal of molecular sciences2023
Effects of Aloe-Emodin on the Expression of Brain Aquaporins and Secretion of Neurotrophic Factors in a Rat Model of Post-Stroke Depression.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Modified Jie-Yu-He-Huan Capsule in Post-Stroke Depression Treatment: Insights from DIA Proteomic and PRM Validation.Drug design, development and therapy · 2026Article
- Post stroke depression: pathogenesis and molecular mechanisms of natural product-based interventions.Frontiers in pharmacology · 2025Review
- Exploration of Potential Targets and Molecular Mechanisms of the Yiqi Jianpi Tongqiao Formula in Treating Allergic Rhinitis Mouse Model based on Network Pharmacology and Molecular Docking.Current computer-aided drug design · 2025Article
- Pharmacology, medical uses, and clinical translational challenges of Saikosaponin A: A review.Heliyon · 2024Review
- Inhibition of SK Channels in VTA Affects Dopaminergic Neurons to Improve the Depression-Like Behaviors of Post-Stroke Depression Rats.Neuropsychiatric disease and treatment · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Post-stroke depression (PSD) is a common complication of stroke that can damage patients' brains. More and more studies have been conducted on PSD in recent years, but the exact mechanism is still not understood. Currently, animal models provide an alternative approach to better understand the pathophysiology of PSD and may also pave the way for the discovery of new treatments for depression. This study investigated the therapeutic effect and mechanism of aloe-emodin (AE) on PSD rats. Previous studies have shown that AE positively affects PSD in rats by improving depression, increasing their activities and curiosities, enhancing the number of neurons, and ameliorating damage to brain tissue. Meanwhile, AE could up-regulate the expression of brain-derived neurotrophic factor (BDNF) and neurotrophic 3 (NTF3), but it could also down-regulate the expression of aquaporins (AQP3, AQP4, and AQP5), glial fibrillary acidic protein (GFAP), and transient receptor potential vanilloid 4 (TRPV4), which is helpful in maintaining homeostasis and alleviating encephaledema. AE may be a prospective solution in the future for the treatment of PSD patients.
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Registered trials
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