[The effect of semax and its C-end peptide PGP on expression of the neurotrophins and their receptors in the rat brain during incomplete global ischemia].
Stavchanskiĭ. V V VV; Tvorogova. T V TV; Botsina. A Iu AIu; Skvortsova. V I VI; Limborskaia. S A SA; Miasoedov. N F NF; Dergunova. L V LV
Key Findings
- Ischemia sharply lowered neurotrophin and receptor gene expression in the rat hippocampus.
- Semax and its PGP fragment reversed this drop, with the biggest effect seen 12 h after the insult, particularly in the hippocampus.
- In the frontal cortex, semax reduced receptor mRNA levels while PGP increased them, showing different regional actions.
Practical Outcomes
- For biohackers, this suggests semax may have neuroprotective properties by enhancing brain‑derived growth factors after stress or injury. However, the data are from rats and do not translate directly into dosing or safety guidelines for humans, so any use should be cautious and based on broader clinical evidence.
Summary
In rats that had a temporary blockage of blood flow to the brain, the peptide semax (and a related short piece called PGP) helped restore the activity of genes that support nerve cell health, especially in the hippocampus, which is important for memory. The effect was strongest about 12 hours after the blockage. While the study is in animals and doesn’t give human dosing, it adds evidence that semax can boost brain‑protective factors after injury.
Abstract
Neurotrophins regulate key function of nervous tissue cells. Analysis of neurotrophins mRNA expression is an appropriate tool to assess therapeutic efficiency of the anti-stroke drugs. We have analyzed the effect of synthetic peptide semax and its C-terminal Pro-Gly-Pro tripeptide upon mRNAs expression of neurotrophins Ngf, Bdrf, Nt-3 and their receptors TrkA, TrkB, TrkC, p75 in rat frontal lobes, hippocampus and cerebellum after bilateral common carotid artery occlusion. The animals were decapitated 30 min, 1, 2, 4, 8, 12, 24 h after the operation. The mRNA expression of neurotrophins and their receptors was assessed by relative quantification using real-time RT-PCR. Our showed that ischemia causes a significant decrease in gene expression in the hippocampus. Semax and PGP affected the expression of neurotrophins and their receptors predominantly in the frontal cortex and hippocampus of the ischemized animals. In the frontal cortex, Semax treatment resulted in a decrease of mRNA level of receptors, while PGP treatment increased the level of these mRNA. Maximal neuroprotective effect of both peptides has been observed in the hippocampus 12 h after occlusion. A decrease of gene expression of neurotrophins and their receptors caused by the occlusion was overcome by Semax and PGP. These results clarify the semax mechanism of and present certain features of mRNA's expression of neurotrophins and their receptors in experimental conditions.
Study Information
pubmed
2011