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

• DOI: 10.1007/s12031-021-01802-0
• Publication Date: 2021-04-13T23:24:25Z
• Authors: Chun Luo; Binru Li; Lang Chen; Lili Zhao; Yinghai Wei
• Keywords: Male; Neurons; STAT3 Transcription Factor; 0301 basic medicine; Interleukin-27; 0303 health sciences; Tumor Necrosis Factor-alpha; Brain; Apoptosis; Infarction, Middle Cerebral Artery; Interleukin-10; 3. Good health; Mice, Inbred C57BL; Mice; 03 medical and health sciences; Neuroprotective Agents; Transforming Growth Factor beta; Cytokine Receptor gp130; Animals; Cells, Cultured; Chemokine CCL2; Signal Transduction

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.