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Brain Protein Expression Profile Confirms the Protective Effect of the ACTH((4-7))PGP Peptide (Semax) in a Rat Model of Cerebral Ischemia-Reperfusion
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study using a transient middle cerebral artery occlusion (tMCAO) model of cerebral ischemia-reperfusion, researchers examined the effect of the peptide Semax (Met-Glu-His-Phe-Pro-Gly-Pro), a synthetic melanocortin derivative, on brain protein expression. At 24 h after tMCAO, Semax was associated with upregulation of active CREB in subcortical structures including the ischemic damage focus, downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex, and downregulation of active JNK in both tissues. The authors also constructed a regulatory network from these findings. They state that suppression of inflammatory and cell death markers alongside activation of CREB-related recovery signaling may contribute to the neuroprotective action of Semax described at both the transcriptome and protein levels.
Abstract
The Semax (Met-Glu-His-Phe-Pro-Gly-Pro) peptide is a synthetic melanocortin derivative that is used in the treatment of ischemic stroke. Previously, studies of the molecular mechanisms underlying the actions of Semax using models of cerebral ischemia in rats showed that the peptide enhanced the transcription of neurotrophins and their receptors and modulated the expression of genes involved in the immune response. A genome-wide RNA-Seq analysis revealed that, in the rat transient middle cerebral artery occlusion (tMCAO) model, Semax suppressed the expression of inflammatory genes and activated the expression of neurotransmitter genes. Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke. At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax. Moreover, a regulatory network was constructed. In conclusion, the suppression of inflammatory and cell death processes and the activation of recovery may contribute to the neuroprotective action of Semax at both the transcriptome and protein levels.
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