IL-27 Protects the Brain from Ischemia-Reperfusion Injury via the gp130/STAT3 Signaling Pathway.

Abstract

The occurrence of ischemia-reperfusion (I/R) injury leads to dysfunction as well as high rates of morbidity and mortality in stroke, and new effective therapeutic strategies for I/R are still needed. We investigated the effect of IL-27 on I/R injury-induced neurological function impairment, cerebral infarction volume and variation in levels of inflammatory factors in mice with middle cerebral artery occlusion (MCAO), as well as concentration of LDH and neuronal apoptosis in a neuron oxygen-glucose deprivation and reperfusion (OGD/R) model mediated by gp130/STAT3 signaling in vitro. Our results indicated that IL-27 could bind to its receptor of gp130 to attenuate the I/R injury-induced impairment function and cerebral infarction volume, and decrease inflammatory cytokines TNF-α, IL-1β and MCP-1 but increase anti-inflammatory factors IL-10 and TGF-β in vivo, while inhibiting LDH leakage and neuronal apoptosis through activation of STAT3 to antagonize I/R induction. Our results suggest that IL-27 may protect the brain from I/R injury through the gp130/STAT3 signaling pathway.

• Authors: Chun Luo, Binru Li, Lang Chen, Lili Zhao, Yinghai Wei
• Journal: Journal of molecular neuroscience : MN (J Mol Neurosci) Vol. 71 Issue 9 Pg. 1838-1848 (Sep 2021) ISSN: 1559-1166 [Electronic] United States
• PMID: 33851350 (Publication Type: Journal Article)
• Copyright: © 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Chemical References

• Ccl2 protein, mouse
• Chemokine CCL2
• Il6st protein, mouse
• Interleukin-27
• Neuroprotective Agents
• STAT3 Transcription Factor
• Stat3 protein, mouse
• Transforming Growth Factor beta
• Tumor Necrosis Factor-alpha
• Interleukin-10
• Cytokine Receptor gp130

Topics

• Animals
• Apoptosis
• Brain (cytology, drug effects, metabolism)
• Cells, Cultured
• Chemokine CCL2 (metabolism)
• Cytokine Receptor gp130 (metabolism)
• Infarction, Middle Cerebral Artery (drug therapy, metabolism)
• Interleukin-10 (metabolism)
• Interleukin-27 (pharmacology, therapeutic use)
• Male
• Mice
• Mice, Inbred C57BL
• Neurons (drug effects, metabolism)
• Neuroprotective Agents (pharmacology, therapeutic use)
• STAT3 Transcription Factor (metabolism)
• Signal Transduction
• Transforming Growth Factor beta (metabolism)
• Tumor Necrosis Factor-alpha (metabolism)