Study summary · research use only
Genes That Associated with Action of ACTH-like Peptides with Neuroprotective Potential in Rat Brain Regions with Different Degrees of Ischemic Damage
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study of transient middle cerebral artery occlusion (tMCAO), the authors examined genes associated with the ACTH-like peptides Semax (ACTH(4-7)PGP) and ACTH(6-9)PGP in the striatum, following earlier RNA-Seq work in the frontal cortex (FC) showing the peptides reduced ischemia-related disturbance profiles for nearly two-thousand differentially expressed genes (DEGs). In the striatum, the peptides generated fewer DEGs than in the FC; both tended to normalize disturbance profiles for hundreds of DEGs, while 152 genes showed a more affected profile under ACTH(6-9)PGP, mainly associated with inflammation. About a hundred genes overlapped between both peptides in both tissues, mainly associated with neuroactive ligand-receptor interaction. The authors describe differential spatial regulation of ischemia-related transcriptome changes across rat brain regions with different injury severity.
Abstract
In the treatment of ischemic stroke, an innovative approach is the use of neuroprotective compounds. Natural peptides, including adrenocorticotropic hormone (ACTH), can serve as the basis for such drugs. Previously, a significant effect of non-hormonal ACTH(4-7)PGP (Semax) and ACTH(6-9)PGP peptides on the functions of the nervous system was shown. Also, while using RNA-Seq, we firstly revealed differentially expressed genes (DEGs) that associated with peptides in the penumbra-associated region of the frontal cortex (FC) of rats at 24 h after transient middle cerebral artery occlusion (tMCAO) model. Peptides significantly reduced profile disturbances caused by ischemia for almost two-thousand DEGs in FC related to the neurotransmitter and inflammatory response. Here, we studied how peptides affected the expression of genes in the striatum with an ischemic focus, predominantly. The same animals from which we previously acquired FC were used to collect striatum samples. Peptides generated fewer DEGs in the striatum than in the FC. Both peptides tended to normalize the profile of disturbances caused by ischemia for hundreds of DEGs, whereas 152 genes showed an even more affected profile in the striatum under ACTH(6-9)PGP action. These DEGs were associated with inflammation, predominantly. About hundred genes were overlapped between both peptides in both tissues and were associated with neuroactive ligand-receptor interaction, predominantly. Thus, genes that are associated with the ACTH-like peptide action in rat brain regions with varying levels of ischemia injury were identified. Moreover, differential spatial regulation of the ischemia process in the rat brain at the transcriptome levels was discovered under peptides with different ACTH structures. We suppose that our results may be useful for selecting more effective neuroprotective drug structures in accordance with their specific tissue/damage therapeutic impact.
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