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Semax research

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NCBI Semax, an analog of ACTH(4-7), controls the expression of immune response genes during ischemic brain damage in rats.
Semax is an artificial peptide that comprises of the N-terminal adrenocorticotropic hormone fragment (4-7) (ACTH4-7) and also C-terminal Pro-Gly-Pro peptide. Semax stimulates neuron survival in hypoxia, intensifies selective memory storage and attention.
Rain stroke keeps claiming the lives of millions of people yearly. To build the efficient approaches for stroke treatment, it is compulsory to understand the neuroprotective mechanisms that can prevent the ischemic injury. Consisting of the ACTH(4-7) fragment and the tripeptide Pro-Gly-Pro (PGP), the synthetic peptide Semax efficiently protects the brain against ischemic stroke. On the other hand, the molecular mechanisms essential to its neuroprotection and contribution of PGP in them are still required to be clarified. To reveal biological processes and signaling pathways, which are affected by Semax and PGP, we performed the transcriptome study of the cerebral cortex of rats with focal cerebral ischemia treated by these peptides. The genome-wide biochip data analysis identified the differentially expressed genes (DEGs), and bioinformatic web-tool Ingenuity iReport found DEGs associations with quite a lot of biological processes and signaling pathways. The immune response is the process that is most markedly affected by the peptide: Semax increases antigen presentation signaling pathway, strengthens the effect of ischemia on the interferon signaling pathways and influences the processes for synthesizing immunoglobulin. Semax expressively increases expression of the gene encoding the immunoglobulin heavy chain, have high effects on cytokine, stress response and ribosomal protein-encoding genes after occlusion. PGP treatment of rats with ischemia weakens the immune activity and suppresses neurotransmission in the CNS. We suppose that neuroprotective mechanism of Semax is appreciated via the neuroimmune crosstalk, and the new properties of PGP were found under ischemia. Our results provided the basis for further proteomic research in the field of Semax neuroprotection mechanism.
KEYWORDS:
ACTH analog; Cerebral ischemia model; Genome-wide transcriptome analysis; Immune response; immunoglobulin; Neuroprotective regulatory peptides; Pro-Gly-Pro; Semax

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