Vinpocetine Inhibits NF-κB-Dependent Inflammation in Acute Ischemic Stroke Patients

Zhang, Fang; Yan, Chen; Wei, Changjuan; Yao, Yang; Ma, Xiaofeng; Gong, Zhongying; Liu, Shoufeng; Zang, Dawei; Chen, Jieli; Shi, Fu‐Dong; Hao, Junwei

doi:10.1007/s12975-017-0549-z

Cited by 70 publications

(52 citation statements)

References 52 publications

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“…During the acute phase of CNS injury, the proliferation of astrocytes occurred which contributed to cell death, neovascular remodeling, multicellular inflammation, loss of axons and synapse in perilesion, and loss of oligodendrocytes . Astrocytes play a primary role in the production of inflammatory cytokines, chemokines, and ROS, leading to the inhibition of oligodendrocyte progenitor differentiation and hydrocephalus, resulting in secondary brain injury . Then newly proliferated and hypertrophic astrocyte cells, fibroblast‐linage cells and inflammatory cells consisted of astrogliosis scar formation under modulating by intrinsic signaling transduction such as STAT3 and NF‐ƙB pathway .…”

Section: Discussionmentioning

confidence: 99%

“…Although previous studies have shown that reactive astrogliosis (also known as astrocyte activation) is necessary for poststroke CNS repair, recent studies have demonstrated that reactive astrogliosis plays a pivotal role in neurological injury in CNS injury models such as hemorrhagic stroke . Reactive astrogliosis is characterized by astrocyte hypertrophy and astrocyte proliferation, which have been shown to contribute to glial scar formation .…”

Section: Introductionmentioning

confidence: 99%

“…Although previous studies have shown that reactive astrogliosis (also known as astrocyte activation) is necessary for poststroke CNS repair, [7][8][9] recent studies have demonstrated that reactive astrogliosis plays a pivotal role in neurological injury in CNS injury models such as hemorrhagic stroke. [10][11][12][13] Reactive astrogliosis is characterized by astrocyte hypertrophy and astrocyte proliferation, which have been shown to contribute to glial scar formation. 14 Despite glial scarring being necessary to seal the site of injury and protect damaged neural tissue, this repair mechanism inhibited the regrowth of damaged axons which contributed to further neurological deficits brought on by CNS injury.…”

Section: Introductionmentioning

confidence: 99%

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Secukinumab attenuates reactive astrogliosis via IL‐17RA/(C/EBPβ)/SIRT1 pathway in a rat model of germinal matrix hemorrhage

et al. 2019

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Aims Reactive astrogliosis plays a critical role in neurological deficits after germinal matrix hemorrhage (GMH). It has been reported that interleukin‐17A and IL‐17A receptor IL‐17RA/(C/EBPβ)/SIRT1 signaling pathway enhances reactive astrogliosis after brain injuries. We evaluated the effects of secukinumab on reactive astrogliosis in a rat pup model of GMH. Methods A total of 146 Sprague Dawley P7 rat pups were used. GMH was induced by intraparenchymal injection of collagenase. Secukinumab was administered intranasally 1 hour post‐GMH. C/EBPβ CRISPR or SIRT1 antagonist EX527 was administrated intracerebroventricularly (icv) 48 hours and 1 hour before GMH induction, respectively. Neurobehavior, Western blot, histology, and immunohistochemistry were used to assess treatment regiments in the short term and long term. Results The endogenous IL‐17A, IL‐17RA, C/EBPβ, and GFAP and proliferation marker CyclinD1 were increased, while SIRT1 expression was decreased after GMH. Secukinumab treatment improved neurological deficits, reduced ventriculomegaly, and increased cortical thickness. Additionally, treatment increased SIRT1 expression and lowered proliferation proteins PCNA and CyclinD1 as well as GFAP expression. C/EBPβ CRISPR activation plasmid and EX527 reversed the antireactive astrogliosis effects of secukinumab. Conclusion Secukinumab attenuated reactive astrogliosis and reduced neurological deficits after GMH, partly by regulating IL‐17RA/(C/EBPβ)/SIRT1 pathways. Secukinumab may provide a promising therapeutic strategy for GMH patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Secukinumab attenuates reactive astrogliosis via IL‐17RA/(C/EBPβ)/SIRT1 pathway in a rat model of germinal matrix hemorrhage

et al. 2019

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“…Response. Inflammatory processes and immunoreaction participate in the pathogenesis of ischemic stroke [100], CHD [101], and depression, and they have common molecules with OS. Inflammation and immune reactions exist in ischemic CVD and depression.…”

Section: Inflammation and Immunementioning

confidence: 99%

The Role of Oxidative Stress in Common Risk Factors and Mechanisms of Cardio-Cerebrovascular Ischemia and Depression

Lin

Wang

Yan

et al. 2019

Oxidative Medicine and Cellular Longevity

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The public health sector faces a huge challenge as a result of the high prevalence and burden of disability caused by ischemic cardio-cerebrovascular disease (CVD) and depression. Although studies have explored the underlying mechanisms and potential therapies to address conditions, there is no treatment breakthrough, especially for depression which is highly influenced by social stressors. However, accumulating evidence reveals that CVD and depression are correlated and share common risk factors, particularly obesity, diabetes, and hypertension. They also share common mechanisms, including oxidative stress (OS), inflammation and immune response, cell death signaling pathway, and microbiome-gut-brain axis. This review summarizes the relationship between ischemic CVD and depression and describes the interactions among common risk factors and mechanisms for these two diseases. In addition, we propose that OS mediates the crosstalk between these diseases. We also reveal the potential of antioxidants to ameliorate OS-related injuries.

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“…Препарат является ингибитором киназы IκB, которая играет важную роль в опосредовании клеточных воспалительных реакций и экспрессии разнообразных провоспалительных медиаторов, включая цитокины, хемокины и молекулы адгезии. Что еще более важно, о противовоспалительном действии винпоцетина свидетельствуют результаты многоцентрового исследования, в котором приняли участие 60 пациентов с инсультом: у получавших винпоцетин наблюдалось лучшее восстановление неврологической функции, что коррелировало с более низким уровнем активации провоспалительных медиаторов [42].…”

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Vascular cognitive impairment and Alzheimer's disease: Is there a relationship between them?

Tabeeva

Kirjanova

2019

RJTAO

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Cognitive impairment (CI) associated with brain aging is a consequence of disorders varying in etiology and pathogenesis, which often coexist in elderly patients and can have a mutual impact on the clinical manifestation, severity, and rate of progression of CI. Alzheimer's disease (AD) and vascular CI are the most common forms of dementia in the elderly. In recent decades, there has been increasing evidence that there is a close relationship between these forms due to a substantial overlap of their risk factors, clinical manifestations, neuromorphological changes, as well as genetic and neuroimaging biomarkers. The complex multicomponent relationship of these disorders also makes it difficult to elaborate effective preventive and therapeutic approaches in these patients.

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Vinpocetine Inhibits NF-κB-Dependent Inflammation in Acute Ischemic Stroke Patients

Abstract: www.clinicaltrials.gov . Identifier: NCT02878772.

Cited by 70 publications

References 52 publications

Secukinumab attenuates reactive astrogliosis via IL‐17RA/(C/EBPβ)/SIRT1 pathway in a rat model of germinal matrix hemorrhage

Secukinumab attenuates reactive astrogliosis via IL‐17RA/(C/EBPβ)/SIRT1 pathway in a rat model of germinal matrix hemorrhage

The Role of Oxidative Stress in Common Risk Factors and Mechanisms of Cardio-Cerebrovascular Ischemia and Depression

Vascular cognitive impairment and Alzheimer's disease: Is there a relationship between them?

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