Selank Peptide Causes Changes in Gene Expression in the Hippocampus of Rats in the Early Hours after Acute Restraint Stress

• Published in: Nanobiotechnology Reports (Online) 2024-06, Vol.19 (3), p.381-392
• Main Authors: Filippenkov, I. B., Glazova, N. Yu, Sebentsova, E. A., Mozgovoy, I. V., Stavchansky, V. V., Myasoedov, N. F., Levitskaya, N. G., Limborska, S. A., Dergunova, L. V.
• Format: Article
• Language: English
• Subjects: Chemistry and Materials Science; Constraints; Gene expression; Gene sequencing; Hippocampus; Industrial and Production Engineering; Machines; Manufacturing; Materials Science; Nanobiology and Genetics; Nanotechnology; Omics Technologies; Peptides; Processes; Ribonucleic acid; RNA
• ISSN: 2635-1676; 1995-0780; 2635-1684; 1995-0799
• DOI: 10.1134/S2635167624601335

Stress is a risk factor for the development of anxiety-depressive disorders, cardiovascular diseases, and cognitive impairment. The peptide drug ThrLysProArgProGlyPro (Selank), an analogue of endogenous tuftsin, has entered clinical practice as an anxiolytic agent acting as a positive allosteric modulator. In a model of acute restraint stress, high-throughput RNA sequencing (RNA-Seq) is used to demonstrate that Selank is able to significantly alter gene expression in the rat hippocampus 2 h after stress exposure. Thus, the introduction of Selank (300 μg/kg) to rats 30 min before the start of immobilization lasting 1 h leads to a change in the expression of 549 genes (fold change >1.5 and Padj < 0.05), which are related to the systems of processing and presentation of antigens and transmission of nerve impulses. At the same time, when Selank is administered to rats in the absence of stress, no significant change in gene expression in the hippocampus is observed. Thus, Selank can regulate the processes caused by acute stress at the molecular-genetic level already in the early hours after acute stress, without affecting genomic activity in the absence of such an impact.