Study summary · research use only
[The Peptide Drug ACTH(4-7)PGP (Semax) Suppresses mRNA Transcripts Encoding Proinflammatory Mediators Induced by Reversible Ischemia of the Rat Brain]
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used a rat model of transient middle cerebral artery occlusion (ischemia-reperfusion) to examine effects of the peptide Semax on gene expression. Building on earlier RNA-Seq analysis showing increased mRNA levels of proinflammatory genes and their suppression by Semax, the authors used qRT-PCR to analyze weakly expressed mRNAs including Il1a, Il1b, Il6, and Tnfa, and report that Semax exposure was associated with a statistically significant decrease in Il1a, Il1b, Il6, Ccl3, and Cxcl2 mRNAs, compensating for the ischemia-reperfusion-induced increase in transcription of these genes. The authors describe the observed protective effect of Semax in this stroke model as possibly related to its anti-inflammatory effects, and discuss limitations of RNA-Seq for quantifying low-abundance transcripts compared with real-time RT-PCR.
Abstract
Due to its nootropic, neuroprotective, and immunomodulatory effects, the peptide Semax is utilized in the treatment of ischemic stroke. Our earlier RNA-Seq analysis of the transcriptome in an ischemic model of transient occlusion of the middle cerebral artery showed an increase in the mRNA levels of many proinflammatory genes, and the suppression of their induction by Semax. However, for many relevant genes, including Il1a, Il1b, Il6 and Tnfa, the levels of their expression were too low for detailed quantitative evaluation. Here we utilize qRT-PCR to analyze the effects of the Semax peptide on the expression of weakly expressed mRNAs encoding several proinflammatory mediators, and show that exposure to Semax leads to a statistically significant decrease in the Il1a, Il1b, Il6, Ccl3, and Cxcl2 mRNAs, which compensates for the increase in the transcription of these genes induced by ischemia-reperfusion. We conclude that the observed protective effect of Semax in the model of stroke may be due to its anti-inflammatory effects. We also discuss the limitations of the RNA-Seq when applied to quantifying less abundant transcripts as compared to the real-time RT-PCR method.
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