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.

缺血再灌注 (I/R) 损伤的发生导致卒中功能障碍以及高发病率和死亡率，仍然需要新的 I/R 有效治疗策略。我们研究了 IL-27 对大脑中动脉闭塞 (MCAO) 小鼠 I/R 损伤引起的神经功能损害、脑梗死体积和炎症因子水平变化以及 LDH 浓度和神经元凋亡的影响。体外由 gp130/STAT3 信号传导介导的神经元氧-葡萄糖剥夺和再灌注 (OGD/R) 模型。我们的研究结果表明，IL-27 可以与其 gp130 受体结合，减轻 I/R 损伤引起的功能障碍和脑梗死体积，并减少炎性细胞因子 TNF-α，IL-1β 和 MCP-1 但在体内增加抗炎因子 IL-10 和 TGF-β，同时通过激活 STAT3 拮抗 I/R 诱导来抑制 LDH 渗漏和神经元凋亡。我们的研究结果表明，IL-27 可能通过 gp130/STAT3 信号通路保护大脑免受 I/R 损伤。