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Information × Registration Number 0224U032361, 0123U101110 , R & D reports Title The role of the thiol-disulfide system in the implementation of neurodestruction/neuroprotection mechanisms and the development of pharmacological modulation pathways after prenatal hypoxia popup.stage_title Вивчення in vitro нейропротекції модуляторів тіол-дисульфідної системи при деривації синтезу відновлених тіолів у суспензії нейронів головного мозку щурят після ПГ Head Belenichev Ihor Fedorovych, Доктор біологічних наук Registration Date 22-09-2024 Organization Zaporizhzhya State Medical University popup.description2  Object of study - hypoxic disorders of prenatal brain development. The aim of the study is to experimentally substantiate the use of thiol-disulfide system modulators (glutaredoxin, thioazotate, L-lysine thioazotate, interleukin-1β receptor antagonist (IL-1ra), and systems that are conjugated to it - HSP70 (L-lysine thioazotate, heat shock factor 1 [HSF-1], tamoxifen, cerebrolysin) and NO system (L-arginine thioazotate, L-lysine thioazotate, mildronate) in the treatment of prenatal CNS hypoxia effects based on experimental data revealing the role of thiol-disulfide system in interrupting NO-, IL-1b-, ROS-dependent mechanisms of neurodegradation and excitotoxicity and SH/HSP70-mediated mechanisms of endogenous neuroprotection regulation. Research methods - pharmacological, biochemical, histological, immunohistochemical, immunoenzymatic, real-time polymerase chain reaction (PCR), immunoblotting, statistical. Research results and their novelty. Using modern biochemical, molecular, immunohistochemical methods of research, as well as PCR, it was first established that prenatal hypoxia inhibits transcriptional processes and synthesis of HIF1a, HSP70 and c-fos in the brain neurons of animals after PG, indicating a violation of the mechanisms of endogenous neuroprotection. For the first time, it was found that chronic PG leads to inhibition of transcriptional processes in neurons and inhibition of HIF-1α, HSP70 and c-fos synthesis, which indicates a violation of endogenous neuroprotection mechanisms. It has been established that the nitric oxide synthase system, namely the part that regulates the expression of nNOS, eNOS, and iNOS mRNA, is an important target for neuroprotection in chronic prenatal hypertension. Chronic prenatal hypoxia leads to a decrease in myocardial contractility and sinus node dysfunction. Product Description popup.authors Aliieva Olena Н. Berest Halyna H. Honcharov Oleksii V. Dmyrtriieva Oksana O. Kozhemiaka Maksym O. Kuchkovskyi Oleh M. Makieieva Liudmyla V. Popazova Olena O. Ryzhenko Viktor P. Salnikov Valerii I. Samura Iryna B. Skoryna Dmytro Yu. popup.nrat_date 2024-10-01 Close
R & D report
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Head: Belenichev Ihor Fedorovych. The role of the thiol-disulfide system in the implementation of neurodestruction/neuroprotection mechanisms and the development of pharmacological modulation pathways after prenatal hypoxia. (popup.stage: Вивчення in vitro нейропротекції модуляторів тіол-дисульфідної системи при деривації синтезу відновлених тіолів у суспензії нейронів головного мозку щурят після ПГ). Zaporizhzhya State Medical University. № 0224U032361
1 documents found

Updated: 2026-03-22