PMID: 34201112
Sudarkina et al./PubMed/2021
Why It Matters
This paper caught my attention because Semax is actually available as a nasal spray in some countries for stroke treatment, but the mechanisms weren't clear. This study provides protein-level evidence (beyond just gene expression) for how it might work — by suppressing inflammation and cell death while promoting recovery. But critical caveat: this is a rat stroke model with measurements at just one timepoint (24 hours). We don't know if these protein changes translate to better functional outcomes or work in human brains.
Key Findings
- 24 hours after stroke, Semax increased active CREB protein in subcortical brain structures including the damaged area — CREB is involved in cell survival and neural recovery
- The peptide decreased MMP-9 (breaks down blood-brain barrier) and c-Fos (inflammatory marker) in the frontoparietal cortex adjacent to stroke damage
- Active JNK protein, which triggers cell death pathways, was reduced in both cortical and subcortical tissues with Semax treatment
- Protein-level changes aligned with previous RNA-Seq data showing Semax suppressed inflammatory genes and activated neurotransmitter genes
- Effects were measured using transient middle cerebral artery occlusion (tMCAO), a standard rat stroke model, with single-dose peptide administration
Read the Paper↗PMID: 34201112