Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia–Reperfusion in Rats
| Autor: | Vasily V. Stavchansky, Olga Yu. Sudarkina, Ivan B. Filippenkov, Lyudmila V. Dergunova, Larisa E. Sevan’kaeva, Veronika G. Dmitrieva, Svetlana A. Limborska, Alina E. Denisova, Nikolai F. Myasoedov, Leonid V. Gubsky, Vadim V. Yuzhakov |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
lcsh:QH426-470 Ischemia Semax synthetic melanocortin derivative ACTH(4-7)PGP (Semax) Neurotransmission Pharmacology Neuroprotection Article Brain Ischemia Transcriptome 03 medical and health sciences 0302 clinical medicine Adrenocorticotropic Hormone Genetics medicine Animals Humans RNA-Seq Gene Genetics (clinical) peptide regulation Chemistry Brain mRNA expression Biological activity Infarction Middle Cerebral Artery medicine.disease Peptide Fragments Rats Disease Models Animal lcsh:Genetics 030104 developmental biology Reperfusion Injury Melanocortin tMCAO 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Genes, Vol 11, Iss 681, p 681 (2020) Genes Volume 11 Issue 6 |
| ISSN: | 2073-4425 |
| Popis: | Cerebral ischaemia is the most common cause of impaired brain function. Biologically active peptides represent potential drugs for reducing the damage that occurs after ischaemia. The synthetic melanocortin derivative, ACTH(4-7)PGP (Semax), has been used successfully in the treatment of patients with severe impairment of cerebral blood circulation. However, its molecular mechanisms of action within the brain are not yet fully understood. Previously, we used the transient middle cerebral artery occlusion (tMCAO) model to study the damaging effects of ischaemia&ndash reperfusion on the brain transcriptome in rats. Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions. We have identified 394 differentially expressed genes (DEGs) (> 1.5-fold change) in the brains of rats at 24 h after tMCAO treated with Semax relative to saline. Following tMCAO, we found that Semax suppressed the expression of genes related to inflammatory processes and activated the expression of genes related to neurotransmission. In contrast, ischaemia&ndash reperfusion alone activated the expression of inflammation-related genes and suppressed the expression of neurotransmission-related genes. Therefore, the neuroprotective action of Semax may be associated with a compensation of mRNA expression patterns that are disrupted during ischaemia&ndash reperfusion conditions. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|