The role of interleukin-17 in epilepsy

An, Jiayin; Li, He; Xia, Demeng; Xu, Bin; Wang, Jiayan; Qiu, Huahui; He, Jialing

doi:10.1016/j.eplepsyres.2022.107001

Cited by 5 publications

(5 citation statements)

References 118 publications

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“…[ 40 ] Notably, the effects of IL-17 on neuroinflammation, blood-brain barrier integrity, and the secretion of neurotransmitters have been identified as crucial factors in the onset and evolution of EP. [ 41 ] The activation of the IL-17 pathway has been indicated to contribute to the epileptogenicity of cortical abnormalities in focal cortical dysplasia, implying that it may be a novel potential target for antiepileptic therapies. [ 42 ] The TNF pathway initiation escalates the concentration of the pro-inflammatory mediator RELA (p65), which promotes neuroinflammation and has a branch involved in regulating apoptosis or necroptosis.…”

Section: Discussionmentioning

confidence: 99%

Understanding the molecular mechanisms of Acori Tatarinowii Rhizoma: Nardostahyos Radix et Rhizoma in epilepsy treatment using network pharmacology and molecular docking

Cheng,

Wang,

Wang

et al. 2024

Medicine

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Acori Tatarinowii Rhizoma (ATR) and Nardostahyos Radix et Rhizoma (NRR) are well-known traditional Chinese medicines that have been extensively used for the treatment of epilepsy (EP). However, the precise molecular mechanism of ATR-NRR action remains unclear because of their intricate ingredients. This study aimed to investigate the underlying mechanism of ATR-NRR in EP treatment using network pharmacology and molecular docking techniques. Herbal medicine and disease gene databases were searched to determine active constituents and shared targets of ATR-NRR and EP. A protein-protein interaction network was constructed using the STRING database, while the Gene Ontology and the Kyoto Encyclopedia of Genes and Genome pathway enrichment were performed using R programming. An ingredient-target-pathway network map was constructed using the Cytoscape software, incorporating network topology calculations to predict active ingredients and hub targets. The binding abilities of active ingredients and hub targets were examined using molecular docking. Nine qualified compounds and 53 common targets were obtained. The prominent active compounds were kaempferol, acacetin, cryptotanshinone, 8-isopentenyl-kaempferol, naringenin, and eudesmin, while the primary targets were RELA, AKT1, CASP3, MAPK8, JUN, TNF, and TP53. Molecular docking analysis revealed that they have substantial binding abilities. These 53 targets were found to influence EP by manipulating PI3K-Akt, IL-17, TNF, and apoptosis signaling pathways. The findings of this study indicate that ATR-NRR functions against EP by acting upon multiple pathways and targets, offering a basis for future study.

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Section: Discussionmentioning

confidence: 99%

Understanding the molecular mechanisms of Acori Tatarinowii Rhizoma: Nardostahyos Radix et Rhizoma in epilepsy treatment using network pharmacology and molecular docking

Cheng,

Wang,

Wang

et al. 2024

Medicine

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“…Accumulated evidences from recent studies support that IL-17 is closely related to epileptogenicity, and the IL-17 signal pathways may be an underlying antiepileptic treatment target ( 5 ). Increased IL-17 results in neuronal hyperexcitability in brain slice cultures ( 55 ).…”

Section: Pro-inflammatory Molecules In Epilepsymentioning

confidence: 99%

“…In variable types of epileptic patients, increased IL-17 in serum or CSF positively associated with seizure severity ( 53 ). A recent research observes that the numbers of IL-17-secreting γδ T cell locating in epileptogenic lesions are closely related to seizure severity ( 5 ). The deletion of IL-17R in KA-induce SE animal model decreases neuronal excitability and alleviates the seizure activity ( 55 ).…”

Section: Pro-inflammatory Molecules In Epilepsymentioning

confidence: 99%

“…This disorder is serious global health issue affecting over 50-70 million people in the world ( 3 ). Even though a huge number of clinical and basic epileptic researches have been done, approximately 60% of epileptic disorders have unknown pathophysiological basis responsible for the occurrence and recurrence of seizures and 30% of epileptic patients still are resistant to the current pharmacotherapies with recurrent seizures throughout life ( 4 , 5 ). As a result of these facts, it requires a more thorough understanding of the pathophysiological mechanisms in epileptogenesis, as well as exploring more effective therapeutic strategies for epileptic patients.…”

Section: Introductionmentioning

confidence: 99%

“…Accumulated evidences show neuroinflammation is involved in neuronal hyperexcitability and epileptic seizures, as well prolonged epileptic seizures can trigger a chain of neuroinflammatory reactions ( 4 , 11 , 12 ). Neuroinflammation and recurrent seizures can be the mutual initiation factors and consequent reactions, which collectively contribute to devastating clinical consequences ( 5 , 13 ). Meanwhile, an increasing body of preclinical researches reveal that the anti-inflammatory therapies specifically targeted a certain inflammatory component are effective and promising in animal models with seizures and epilepsy ( 14 – 16 ).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Neuroinflammation in epileptogenesis: from pathophysiology to therapeutic strategies

Li,

Wu,

Zeng

et al. 2023

Front. Immunol.

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Epilepsy is a group of enduring neurological disorder characterized by spontaneous and recurrent seizures with heterogeneous etiology, clinical expression, severity, and prognosis. Growing body of research investigates that epileptic seizures are originated from neuronal synchronized and excessive electrical activity. However, the underlying molecular mechanisms of epileptogenesis have not yet been fully elucidated and 30% of epileptic patients still are resistant to the currently available pharmacological treatments with recurrent seizures throughout life. Over the past two decades years accumulated evidences provide strong support to the hypothesis that neuroinflammation, including microglia and astrocytes activation, a cascade of inflammatory mediator releasing, and peripheral immune cells infiltration from blood into brain, is associated with epileptogenesis. Meanwhile, an increasing body of preclinical researches reveal that the anti-inflammatory therapeutics targeting crucial inflammatory components are effective and promising in the treatment of epilepsy. The aim of the present study is to highlight the current understanding of the potential neuroinflammatory mechanisms in epileptogenesis and the potential therapeutic targets against epileptic seizures.

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