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  • Hindawi Limited  (2)
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  • Hindawi Limited  (2)
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  • 1
    Online Resource
    Online Resource
    Network Pharmacology and Bioinformatics Methods Reveal the Mechanism of Berberine in the Treatment of Ischaemic Stroke
    Hindawi Limited ; 2022
    In:  Evidence-Based Complementary and Alternative Medicine Vol. 2022 ( 2022-6-29), p. 1-17
    Details
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2022 ( 2022-6-29), p. 1-17
    Abstract: Aim. To elucidate the mechanism of action of berberine on ischaemic stroke based on network pharmacology, bioinformatics, and experimental verification. Methods. Berberine-related long noncoding RNAs (lncRNAs) were screened from public databases. Differentially expressed lncRNAs in ischaemic stroke were retrieved from the Gene Expression Omnibus (GEO) database. GSE102541 was comprehensively analysed using GEO2R. The correlation between lncRNAs and ischaemic stroke was evaluated by the mammalian noncoding RNA-disease repository (MNDR) database. The component-target-disease network and protein-protein interaction (PPI) network of berberine in the treatment of ischaemic stroke were constructed by using network pharmacology. We then performed gene ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analyses. Finally, according to the molecular docking analysis and the binding probability between the lncRNA and key proteins, the effectiveness of the results was further verified by in vitro experiments. Results. After matching stroke-related lncRNAs with berberine-related lncRNAs, four genes were selected as potential targets of berberine in the treatment of ischaemic stroke. Subsequently, lncRNA H19 was identified as the potential crucial regulatory lncRNA of berberine. Here, 52 target proteins of berberine in the treatment of ischaemic stroke were identified through database mining. Through topological analysis, 20 key targets were identified which were enriched in inflammation, apoptosis, and immunity. Molecular docking results showed that MAPK8, JUN, and EGFR were central genes. Finally, in vitro experiments demonstrated that lncRNA H19, p-JNK1/JNK1, p-c-Jun/c-Jun, and EGFR expressions were significantly increased in hypoxia-treated SH-SY5Y cells and were restored by berberine treatment. Conclusion. The potential targets and biological effects of berberine in the treatment of ischaemic stroke were predicted in this study. The lncRNA H19/EGFR/JNK1/c-Jun signalling pathway may be a key mechanism of berberine-induced neuroprotection in ischaemic stroke.
    Type of Medium: Online Resource
    ISSN: 1741-4288 , 1741-427X
    URL: Article
    DOI: 10.1155/2022/5160329
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2148302-4
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases
    Hindawi Limited ; 2020
    In:  Oxidative Medicine and Cellular Longevity Vol. 2020 ( 2020-07-03), p. 1-27
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2020 ( 2020-07-03), p. 1-27
    Abstract: The blood-brain barrier (BBB), as a crucial gate of brain-blood molecular exchange, is involved in the pathogenesis of multiple neurological diseases. Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the scavenger system. Since oxidative stress plays a significant role in the production and maintenance of the BBB, the cerebrovascular system is especially vulnerable to it. The pathways that initiate BBB dysfunction include, but are not limited to, mitochondrial dysfunction, excitotoxicity, iron metabolism, cytokines, pyroptosis, and necroptosis, all converging on the generation of ROS. Interestingly, ROS also provide common triggers that directly regulate BBB damage, parameters including tight junction (TJ) modifications, transporters, matrix metalloproteinase (MMP) activation, inflammatory responses, and autophagy. We will discuss the role of oxidative stress-mediated BBB disruption in neurological diseases, such as hemorrhagic stroke, ischemic stroke (IS), Alzheimer’s disease (AD), Parkinson’s disease (PD), traumatic brain injury (TBI), amyotrophic lateral sclerosis (ALS), and cerebral small vessel disease (CSVD). This review will also discuss the latest clinical evidence of potential biomarkers and antioxidant drugs towards oxidative stress in neurological diseases. A deeper understanding of how oxidative stress damages BBB may open up more therapeutic options for the treatment of neurological diseases.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2020/4356386
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2455981-7
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