Semax · research summary

Genes That Associated with Action of ACTH-like Peptides with Neuroprotective Potential in Rat Brain Regions with Different Degrees of Ischemic Damage.

International journal of molecular sciences · 2025. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

Preclinical animal study using RNA-Seq and histology to analyze gene expression in rat brain after ischemic stroke and peptide administration.
“Here, using RNA-Seq we aimed to study the effect of Semax and ACTH(6-9)PGP peptides on gene expression in the ischemia focus-containing striatum.”

Subjects

Male Wistar rats subjected to transient middle cerebral artery occlusion (tMCAO).
“The Wistar line of white male rats, weighing between 200 and 250 g, were acquired from AlCondi, Ltd. (Moscow, Russia), as previously mentioned [25].”

Sample size

At least five animals per experimental group for the main study, with n=3 animals per group used for RNA-Seq analysis and n=5 for RT-PCR validation.
“At least five animals were included in each experimental group.”

Duration

24 hours after the transient middle cerebral artery occlusion (tMCAO) procedure.
“At 24 h after the beginning of the tMCAO/sham operation, the rats were decapitated.”

Reported findings

Peptides generated fewer differentially expressed genes (DEGs) in the striatum than in the frontal cortex, with the transcriptomic effect being more extensive in the penumbra-associated frontal cortex.
“At 24 h after tMCAO, the transcriptomic effect of peptides in the penumbra-associated FC was much more extensive than in the infarct-associated striatum.”
Semax exhibited a predominantly compensatory effect in the striatum, normalizing gene expression profiles disturbed by ischemia.
“In striatum, the effect of Semax was predominantly compensatory and aimed at reducing the effect of ischemia.”
ACTH(6-9)PGP showed a heterogeneous effect in the striatum, enhancing the impact of ischemia on genes associated with inflammation in addition to compensatory effects.
“Concomitantly, ACTH(6-9)PGP peptide was able to enhance the effect of ischemia on many genes, in addition to the compensatory effect.”

Limitations stated by the authors

The study was conducted in rats, and the authors note that further protein studies are required to translate genome effects into phenotype meaning and clinical application.
“Further protein studies would be significant for translating genome effects into phenotype meaning and into clinical application as well.”

Source: PubMed 40650034 · DOI 10.3390/ijms26136256 · all study summaries

Reported findings

Peptides generated fewer differentially expressed genes (DEGs) in the striatum than in the frontal cortex, with the transcriptomic effect being more extensive in the penumbra-associated frontal cortex.

“At 24 h after tMCAO, the transcriptomic effect of peptides in the penumbra-associated FC was much more extensive than in the infarct-associated striatum.”

Semax exhibited a predominantly compensatory effect in the striatum, normalizing gene expression profiles disturbed by ischemia.

“In striatum, the effect of Semax was predominantly compensatory and aimed at reducing the effect of ischemia.”

ACTH(6-9)PGP showed a heterogeneous effect in the striatum, enhancing the impact of ischemia on genes associated with inflammation in addition to compensatory effects.

“Concomitantly, ACTH(6-9)PGP peptide was able to enhance the effect of ischemia on many genes, in addition to the compensatory effect.”

Limitations stated by the authors

The study was conducted in rats, and the authors note that further protein studies are required to translate genome effects into phenotype meaning and clinical application.

“Further protein studies would be significant for translating genome effects into phenotype meaning and into clinical application as well.”