Study summary · research use only
Novel Insights into the Protective Properties of ACTH((4-7))PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, researchers used RNA sequencing to examine how the synthetic peptide ACTH(4-7)PGP (Semax) affects the brain transcriptome after transient middle cerebral artery occlusion, a model of cerebral ischaemia-reperfusion. The abstract reports that Semax treatment was associated with differentially expressed genes in rat brains compared to saline treatment. Following the ischaemia model, Semax was reported to suppress expression of genes related to inflammatory processes and activate expression of genes related to neurotransmission, whereas ischaemia-reperfusion alone was associated with the opposite pattern, activating inflammation-related genes and suppressing neurotransmission-related genes. The authors describe the neuroprotective action of Semax as potentially linked to compensation of mRNA expression patterns disrupted during ischaemia-reperfusion.
Abstract
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-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-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-reperfusion conditions.
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