Study summary · research use only
[POSSIBLE ROLE OF TRANSTHYRETIN IN THE BIOLOGICAL MECHANISM OF THE REGULATORY PEPTIDE NEUROPROTECTION.]
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses the peptide preparation Semax, used in ischemic stroke therapy, and its possible neuroprotection mechanism via the protein transthyretin (Ttr), drawing on a prior full-genome transcriptome analysis in rat brain. It reports that under focal ischemia of rat brain, Semax modified the transcription activity profile of many genes, and that the difference in transcription levels of the Ttr-encoding gene between ischemic and Semax-treated rats was very high. Citing high similarity between the effects of Ttr and coupled molecular systems and the effects of Semax in ischemic stroke, the authors suggest that Semax's neuroprotection mechanisms could be mediated by Ttr, and the review discusses Ttr's role in the central nervous system (CNS) and its possible role in the neuroprotection mechanism of Semax.
Abstract
The peptide preparation Semax has been effectively used for therapy of ischemic stroke. However, the mechanisms of its action are insufficiently understood and actively studied. The full-genome analysis of the transcriptome implemented in our recent work dem- onstrated that under conditions of focal ischemia of rat brain the Semax modified the profile of the transcription activity of many genes. In this case, the difference in the transcription levels of the gene encoding the protein transthyretin (Ttr) expression in rats under the pathological conditions of ischemia and in the presence of Semax was very high. High similarity between the effects of Ttr and coupled molecular systems with the Semax effects in ischemic stroke allowed us to suggest that the neuroprotection mechanisms of Semax (and, possibly, of other neuroprotection mechanisms of Semax) could be mediated by Ttr. In this review, we discussed the role of Ttr in CNS and its possible role in the neuroprotection mechanism of Semax.
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