ArticleCytoJournal2025
Oxoglutarate dehydrogenase-like may alleviate the inflammatory response process of epilepsy by inhibiting JAK/STAT signaling pathway through upregulating collagen type IV alpha 2.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Despite the availability of many epilepsy drugs, certain epilepsy patients still cannot be treated with medication. The dysfunction of oxoglutarate dehydrogenase-like (OGDHL) is related to neurodegeneration. This article aimed to explore the role of OGDHL on interleukin (IL)-1β-induced epileptic cell model and its molecular mechanism. Material and Methods: An epileptic cell model was established using IL-1β. Quantitative real-time polymerase chain reaction was used to detect the expression levels of tumor necrosis factor-α, IL-1β, and IL-6 after different treatments. Western blot was used to detect the recovery effect of OGDHL overexpression on the IL-1-induced epilepsy model of CTX-TNA cells through the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway and collagen type IV alpha 2 (COL4A2) expression level. Meanwhile, the hypertrophy, viability, and apoptosis of CTX-TNA cells were = evaluated through terminal deoxynucleotidyl transferase dUTP nick end labeling staining, cell counting kit-8 assay, and glial fibrillary acidic protein expression. In addition, we evaluated the effect of the JAK/STAT signaling pathway agonist α7nAchR on the effects of OGDHL overexpression. The influence and possible mechanisms of OGDHL overexpression were comprehensively assessed through the above experimental methods. Results: Our results suggest that OGDHL overexpression can alleviate IL-1β-induced inflammatory response to epilepsy through the JAK/STAT signaling pathway and significant upregulation of COL4A2 expression level ( Conclusion: ODGHL overexpression may inhibit the JAK/STAT signaling pathway by upregulating COL4A2 expression, and it inhibited the IL-1β-induced inflammation of CTX-TNA cells in an epileptic model.
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