The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis.
Medvedeva. Ekaterina V EV; Dmitrieva. Veronika G VG; Povarova. Oksana V OV; Limborska. Svetlana A SA; Skvortsova. Veronika I VI; Myasoedov. Nikolay F NF; Dergunova. Lyudmila V LV
Key Findings
- Semax strongly increases expression of immune‑related genes (immunoglobulins, chemokines) after brain ischemia.
- It also alters a smaller set of vascular‑related genes that control endothelial and smooth‑muscle cell growth and blood‑vessel formation.
- The gene‑expression changes are larger at 24 hours than at 3 hours post‑stroke, indicating a time‑dependent response.
Practical Outcomes
- For biohackers, the study suggests Semax may have immune‑modulating and vascular‑supporting actions that could contribute to brain protection, but the data are from rats with induced strokes and not directly translatable to healthy humans. No dosage or protocol guidance is provided, so any use would be experimental and should be approached with caution.
Summary
In rats that had a small stroke, the peptide Semax changed the activity of many genes, especially those involved in the immune system and blood‑vessel formation. The biggest changes were seen a day after the stroke, with more immune‑related genes turned on and some genes that help blood vessels grow also affected. The researchers think these immune and vascular effects help protect the brain.
Abstract
The nootropic neuroprotective peptide Semax (Met-Glu-His-Phe-Pro-Gly-Pro) has proved efficient in the therapy of brain stroke; however, the molecular mechanisms underlying its action remain obscure. Our genome-wide study was designed to investigate the response of the transcriptome of ischemized rat brain cortex tissues to the action of Semax in vivo. The gene-expression alteration caused by the action of the peptide Semax was compared with the gene expression of the "ischemia" group animals at 3 and 24 h after permanent middle cerebral artery occlusion (pMCAO). The peptide predominantly enhanced the expression of genes related to the immune system. Three hours after pMCAO, Semax influenced the expression of some genes that affect the activity of immune cells, and, 24 h after pMCAO, the action of Semax on the immune response increased considerably. The genes implicated in this response represented over 50% of the total number of genes that exhibited Semax-induced altered expression. Among the immune-response genes, the expression of which was modulated by Semax, genes that encode immunoglobulins and chemokines formed the most notable groups. In response to Semax administration, 24 genes related to the vascular system exhibited altered expression 3 h after pMCAO, whereas 12 genes were changed 24 h after pMCAO. These genes are associated with such processes as the development and migration of endothelial tissue, the migration of smooth muscle cells, hematopoiesis, and vasculogenesis. Semax affects several biological processes involved in the function of various systems. The immune response is the process most markedly affected by the drug. Semax altered the expression of genes that modulate the amount and mobility of immune cells and enhanced the expression of genes that encode chemokines and immunoglobulins. In conditions of rat brain focal ischemia, Semax influenced the expression of genes that promote the formation and functioning of the vascular system.The immunomodulating effect of the peptide discovered in our research and its impact on the vascular system during ischemia are likely to be the key mechanisms underlying the neuroprotective effects of the peptide.
Study Information
pubmed
2014
2014-03-24T00:00:00.000Z
10.1186/1471-2164-15-228
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