Prenatal hypoxia (PH) causes pathological changes in the brain and can lead to irreversible long-term disorders of its development and the emergence of neuropsychiatric pathologies in children. Pharmacological correction of posthypoxic CNS disorders is a priority problem in modern medicine. The aim of this research was to study the neuroprotective action of drugs with an evidence-based effect on the expression – angiolin, thiotriazoline, tamoxifen, glutoredoxin, cerebrocurin, mexidol and L-arginine in comparison with the reference drug piracetam in terms of their effect on the expression of endogenous neuroprotection factors to further substantiate their use in the treatment of prenatal CNS damage in a model of chronic hemic PH. Expression levels of mRNA HSP70, HIF-1, c-fos and the content of HSP70 in the cytoplasmic and mitochondrial fractions of the brain of rat on the 60th day of life after PH were determined by real-time PCR and enzyme immunoassay. It has been established that chronic PH production inhibits transcriptional processes in neurons and suppresses the synthesis of HIF1a, HSP70 and c-fos. The studied drugs are able to modulate HSP70-mediated mechanisms of endogenous neuroprotection. The most active among HSP70 modulators in conditions of chronic PH are cerebrocurin (150 µl/kg) and angiolin (50 mg/kg), which outperform other studied drugs in terms of increased expression of HSP70, mRNA, HIF-1α mRNA, and HSP70, protein concentration in the brain of experimental animals and can be considered as promising neuroprotective agents in complex therapy after PH.
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SEARCH FOR NEW TARGET LINKS IN COMPLEX THERAPY OF PRENATAL CNS DAMAGE. PHARMACOLOGICAL MODULATION OF HSP70 – DEPENDENT MECHANISMS OF ENDOGENOUS NEUROPROTECTION
Published: 07 November 2022 by MDPI in 8th International Electronic Conference on Medicinal Chemistry session Biomolecules as therapeutics
https://doi.org/10.3390/ECMC2022-13500 (registering DOI)
Keywords: CNS, prenatal hypoxia, endogenous neuroprotection, HSP70