ArticleExperimental and therapeutic medicine2019
Scutellarin-treated exosomes increase claudin 5, occludin and ZO1 expression in rat brain microvascular endothelial cells.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Herbal medicines for SOD1Frontiers in immunology · 2024Pooled it
- Metabolic toxicity and neurological dysfunction in methylmalonic acidemia: from mechanisms to therapeutics.Molecular medicine (Cambridge, Mass.) · 2025Review
- Scutellarin: pharmacological effects and therapeutic mechanisms in chronic diseases.Frontiers in pharmacology · 2024Review
- Exosomes Interactions with the Blood-Brain Barrier: Implications for Cerebral Disorders and Therapeutics.International journal of molecular sciences · 2023Review
- Effect of plasma exosomes on endothelial cell tight junction proteins in SLE patients with immune thrombocytopenia.Clinical rheumatology · 2021Article
- Extracellular Vesicle Proteome of Breast Cancer Patients with and Without Cognitive Impairment Following Anthracycline-based Chemotherapy: An Exploratory Study.Biomarker insights · 2021Article
Corrections and comments
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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
Homocysteine has been reported to be an independent risk factor for stroke. Scutellarin (Scu) dilates cerebral blood vessels and promotes anti-platelet aggregation; however, the mechanism by which Scu and Scu-treated exosomes protect against cerebrovascular disease is unclear. The aim of the present study was to investigate the mechanisms underlying the effects of Scu and Scu-treated exosomes on tight junction proteins in the blood-brain barrier. Rat brain microvascular endothelial cells (RBMVECs) were cultured and divided into five groups: Control, model, Scu, exosomes derived from RBMVECs and exosomes derived from RBMVECs after Scu administration. MTT, lactate dehydrogenase (LDH) and nitric oxide (NO) assays were performed to assess cell viability and injury. Reactive oxygen species (ROS) levels were detected using spectrophotometry and immunofluorescence. Western blotting and immunofluorescence were performed to measure cluster of differentiation (CD) 63, claudin 5, occludin and tight junction protein 1 (ZO1) expression. The results revealed that treatment with Scu and Scu-treated exosomes enhanced cell viability, reduced cell injury, increased NO levels, upregulated CD63, claudin 5, occludin and ZO1, and decreased LDH and ROS levels. These data suggest that Scu and Scu-treated exosomes protect homocysteine-induced RBMVECs via increased claudin 5, occludin and ZO1 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.