Study summary · research use only
Synthetic Adrenocorticotropic Peptides Modulate the Expression Pattern of Immune Genes in Rat Brain following the Early Post-Stroke Period
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in rats used a transient middle cerebral artery occlusion (tMCAO) model of ischemic stroke to examine two synthetic derivatives of adrenocorticotropic hormone (ACTH): ACTH(4-7)PGP (Semax) and ACTH(6-9)PGP. Using RNA-Seq, the authors identified differentially expressed genes in the frontal cortex 4.5 h after tMCAO, including 131 genes related to the first peptide and 322 related to the second. Both Semax and ACTH(6-9)PGP partially prevented ischemia-related changes in immune- and neurosignaling-related gene expression profiles at 4.5 h, though their effects on immune-related genes differed. The authors describe this as providing insight into how the transcriptome depends on peptide structure, relevant to early post-stroke therapy.
Abstract
Ischemic stroke is an acute local decrease in cerebral blood flow due to a thrombus or embolus. Of particular importance is the study of the genetic systems that determine the mechanisms underlying the formation and maintenance of a therapeutic window (a time interval of up to 6 h after a stroke) when effective treatment can be provided. Here, we used a transient middle cerebral artery occlusion (tMCAO) model in rats to study two synthetic derivatives of adrenocorticotropic hormone (ACTH). The first was ACTH(4-7)PGP, which is known as Semax. It is actively used as a neuroprotective drug. The second was the ACTH(6-9)PGP peptide, which is elucidated as a prospective agent only. Using RNA-Seq analysis, we revealed hundreds of ischemia-related differentially expressed genes (DEGs), as well as 131 and 322 DEGs related to the first and second peptide at 4.5 h after tMCAO, respectively, in dorsolateral areas of the frontal cortex of rats. Furthermore, we showed that both Semax and ACTH(6-9)PGP can partially prevent changes in the immune- and neurosignaling-related gene expression profiles disturbed by the action of ischemia at 4.5 h after tMCAO. However, their different actions with regard to predominantly immune-related genes were also revealed. This study gives insight into how the transcriptome depends on the variation in the structure of the related peptides, and it is valuable from the standpoint of the development of measures for early post-stroke therapy.
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