Publications by authors named "R S Esanov"

The goal of this study is to obtain and characterize the complex of quercetin with glycyrrhizic acid, which is known to serve as a drug delivery system. Quercetin is a flavonoid with a wide range of biological activities, including an antimicrobial effect. However, quercetin instability and low bioavailability that limits its use in medical practice makes it necessary to look for new nanoformulations of it.

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We studied the effects of glycyrrhetinic acid (bioactive aglycone of glycyrrhizin) and its ester derivatives at positions C-3 and C-30 on the cell volume regulation in rat thymocytes under conditions of hypoosmotic stress. Native glycyrrhetinic acid completely suppressed this process with half-maximal concentration of 12.7±1.

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A GGGGCC hexanucleotide repeat expansion (HRE) in the C9ORF72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), fatal neurodegenerative diseases with no cure or approved treatments that substantially slow disease progression or extend survival. Mechanistic underpinnings of neuronal death include C9ORF72 haploinsufficiency, sequestration of RNA-binding proteins in the nucleus, and production of dipeptide repeat proteins. Here, we used an adeno-associated viral vector system to deliver CRISPR/Cas9 gene-editing machineries to effectuate the removal of the HRE from the C9ORF72 genomic locus.

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Medical nutrients obtained from plants have been used in traditional medicine since ancient times, owning to the protective and therapeutic properties of plant extracts and products. Glycyrrhizic acid is one of those that, apart from its therapeutic effect, may contribute to stronger bones, inhibiting bone resorption and improving the bone structure and biomechanical strength. In the present study, we investigated the effect of a bioactive glass (BG) addition to the structure-property relationships of supramolecular assemblies formed by glycyrrhizic acid (GA) and its monoammonium salt (MSGA).

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Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease with available treatments only marginally slowing progression or improving survival. A hexanucleotide repeat expansion mutation in the gene is the most commonly known genetic cause of both sporadic and familial cases of ALS and frontotemporal dementia (FTD). The expansion mutation produces five dipeptide repeat proteins (DPRs), and while the mechanistic determinants of DPR-mediated neurotoxicity remain incompletely understood, evidence suggests that disruption of nucleocytoplasmic transport and increased DNA damage contributes to pathology.

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