Diprotin A TFA Exerts Neurovascular Protection in Ischemic Cerebral Stroke

Zhou, Mingyue; Zhang, Yajie; Ding, Hongmei; Wu, Weifeng; Cai, Weiwei; Wang, Yanqiang; Geng, Deqin

doi:10.3389/fnins.2022.861059

Cited by 4 publications

(9 citation statements)

References 36 publications

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“…Different strategies have been employed to improve the BBB penetration proficiency of NPs. Among various approaches, − a common way is to regulate the Wnt/β-catenin signaling produced by glial cells and reduce their binding to multiprotein receptor complexes on brain ECs for cargo administration with high BBB penetration potential. The main limitation of all these methods, however, could be the structural damage and, hence, the dysfunction of the BBB.…”

Section: Properties Affecting Nanoparticle Crossing Through the Bbbmentioning

confidence: 99%

Functionalized Nanomaterials Capable of Crossing the Blood–Brain Barrier

Zha,

Liu,

et al. 2024

ACS Nano

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The blood−brain barrier (BBB) is a specialized semipermeable structure that highly regulates exchanges between the central nervous system parenchyma and blood vessels. Thus, the BBB also prevents the passage of various forms of therapeutic agents, nanocarriers, and their cargos. Recently, many multidisciplinary studies focus on developing cargo-loaded nanoparticles (NPs) to overcome these challenges, which are emerging as safe and effective vehicles in neurotheranostics. In this Review, first we introduce the anatomical structure and physiological functions of the BBB. Second, we present the endogenous and exogenous transport mechanisms by which NPs cross the BBB. We report various forms of nanomaterials, carriers, and their cargos, with their detailed BBB uptake and permeability characteristics. Third, we describe the effect of regulating the size, shape, charge, and surface ligands of NPs that affect their BBB permeability, which can be exploited to enhance and promote neurotheranostics. We classify typical functionalized nanomaterials developed for BBB crossing. Fourth, we provide a comprehensive review of the recent progress in developing functional polymeric nanomaterials for applications in multimodal bioimaging, therapeutics, and drug delivery. Finally, we conclude by discussing existing challenges, directions, and future perspectives in employing functionalized nanomaterials for BBB crossing.

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Section: Properties Affecting Nanoparticle Crossing Through the Bbbmentioning

confidence: 99%

Functionalized Nanomaterials Capable of Crossing the Blood–Brain Barrier

Zha,

Liu,

et al. 2024

ACS Nano

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“…Для анализа и подтверждения повреждения мозга на клеточном уровне используют классические гистологические методы, такие как морфометрическое исследование фиксированных срезов головного мозга, окрашенных толуидиновым синим или крезиловым фиолетовым (по Нисслю), или гематоксилином и эозином [9,27,[40][41][42]. Была продемонстрирована корреляция между объемом повреждения, выявляемом с помощью МРТ и с помощью гистологических методов [9,18,27].…”

Section: методы исследования головного мозга при моделировании инсуль...unclassified

“…Для более точного анализа можно дополнительно использовать методы иммуногистохимического окрашивания, которые позволяют обнаружить нейроны и глиальные клетки и выявить их гибель или пролиферацию. Так, белок NeuN является маркером зрелых нейронов, он используется для визуализации и анализа зоны инфаркта, а также для оценки гибели нейронов [7,17,40,42]. Для выявления зоны пенумбры используют такие маркеры, как c-fos и heart shock protein 90 [9].…”

Section: методы исследования головного мозга при моделировании инсуль...unclassified

“…Нарушение проницаемости гематоэнцефалического барьера (ГЭБ) оценивают с использованием гистохимических красителей, в частности, Эванс Блю (Evans Blue) [17,40]. Известно, что красители, связанные с сывороточным альбумином, могут преодолевать ГЭБ после ишемии.…”

Section: методы исследования головного мозга при моделировании инсуль...unclassified

“…У мышей с фототромботическим кортикальным инсультом также отмечено повреждение нейронов поля СА1 гиппокампа через 28 дней после воздействия по сравнению с ложнооперированными животными [40].…”

Section: морфологические изменения в головном мозге после фтиunclassified

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Photochemicallly Induced Thrombosis as a Model of Ischemic Stroke

Острова

Babkina

Lyubomudrov

et al. 2023

Obŝaâ reanimatologiâ

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Better understanding of ischemic brain injury mechanisms is important for the development and improvement of diagnostic and therapeutic modalities for management of ischemic stroke. As experimental studies are on demand, there’s a need for relevant models of focal brain lesions. Photochemically induced thrombosis remains one of the most popular models of ischemic stroke.The purpose of the review is to consider the pathogenesis and applicational relevance of the photochemical thrombosis in ischemic stroke modeling.Material and methods. The information was searched using PubMed and Google Scholar databases and keywords «photothrombotic stroke» without language restrictions. 74 papers out of more than 600 sources were found the most relevant for the purpose of this review and selected for the analysis. Of these, more than 50% have been published in the last five years. The criterion for excluding a source was an inconsistency with the objectives of the review and low information content.Results. We outlined a variety of features in modeling photothrombotic stroke, analyzed the advantages and disadvantages of the model, presented data on current method’s modifications, as well as approaches to evaluation of brain lesions in ischemic stroke induced by photothrombosis, and summarized information about the mechanisms of brain damage induced in this model.Conclusion. Several advantages of the photothrombotic stroke model, such as low invasiveness, high reproducibility, inherent control of brain infarction volume and low mortality, determine its active use in experimental studies of ischemic stroke. Pathological processes in the brain modeled by photochemical thrombosis are similar to the processes occurring in acute ischemic cerebral circulation events. Therefore, this model provides insights into cellular and molecular mechanisms of ischemic brain damage, and can be used for developing novel therapeutic approaches for management of ischemic stroke.

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Neuroprotective Effect of Hydrogen Sulfide Subchronic Treatment Against TBI-Induced Ferroptosis and Cognitive Deficits Mediated Through Wnt Signaling Pathway

Chen,

et al. 2023

Cell Mol Neurobiol

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Emerging evidence shows that targeting ferroptosis may be a potential therapeutic strategy for treating traumatic brain injury (TBI). Hydrogen sulfide (H2S) has been proven to play a neuroprotective role in TBI, but little is known about the effects of H2S on TBI-induced ferroptosis. In addition, it is reported that the Wnt signaling pathway can also actively regulate ferroptosis. However, whether H2S inhibits ferroptosis via the Wnt signaling pathway after TBI remains unclear. In this study, we first found that in addition to alleviating neuronal damage and cognitive impairments, H2S remarkably attenuated abnormal iron accumulation, decreased lipid peroxidation, and improved the expression of glutathione peroxidase 4, demonstrating the potent anti-ferroptosis action of H2S after TBI. Moreover, Wnt3a or liproxstatin-1 treatment obtained similar results, suggesting that activation of the Wnt signaling pathway can render the cells less susceptible to ferroptosis post-TBI. More importantly, XAV939, an inhibitor of the Wnt signaling pathway, almost inversed ferroptosis inactivation and reduction of neuronal loss caused by H2S treatment, substantiating the involvement of the Wnt signaling pathway in anti-ferroptosis effects of H2S. In conclusion, the Wnt signaling pathway might be the critical mechanism in realizing the anti-ferroptosis effects of H2S against TBI. Graphical Abstract TBI induces ferroptosis-related changes characterized by iron overload, impaired antioxidant system, and lipid peroxidation at the chronic phase after TBI. However, NaHS subchronic treatment reduces the susceptibility to TBI-induced ferroptosis, at least partly by activating the Wnt signaling pathway.

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Diprotin A TFA Exerts Neurovascular Protection in Ischemic Cerebral Stroke

Cited by 4 publications

References 36 publications

Functionalized Nanomaterials Capable of Crossing the Blood–Brain Barrier

Functionalized Nanomaterials Capable of Crossing the Blood–Brain Barrier

Photochemicallly Induced Thrombosis as a Model of Ischemic Stroke

Neuroprotective Effect of Hydrogen Sulfide Subchronic Treatment Against TBI-Induced Ferroptosis and Cognitive Deficits Mediated Through Wnt Signaling Pathway

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