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白细胞介素-27缺失在脑梗死急性缺血期具有神经保护作用。

Interleukin-27 deletion has neuroprotective effects in the acute ischemic stage of cerebral infarction.

作者信息

Furukawa Takashi, Miyake Yasunobu, Ito Hiroshi, Ogata Atsushi, Maeyama Hajime, Nakahara Yukiko, Yoshioka Fumitaka, Masuoka Jun, Yoshida Hiroki, Abe Tatsuya

机构信息

Department of Neurosurgery, Saga University, Faculty of Medicine, Saga, Japan; Department of Biomolecular Sciences, Division of Molecular and Cellular Immunoscience, Saga University, Faculty of Medicine, Saga, Japan.

Department of Biomolecular Sciences, Division of Molecular and Cellular Immunoscience, Saga University, Faculty of Medicine, Saga, Japan.

出版信息

Biochem Biophys Res Commun. 2025 Apr 1;755:151581. doi: 10.1016/j.bbrc.2025.151581. Epub 2025 Mar 5.

Abstract

Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. Cytokines such as interleukins 17 and 23 (IL-17, IL-23) have been involved in stroke. IL-27 is a member of the IL-12 family that consists of IL-27p28 and Epstein-Barr virus-induced gene 3 (EBI3), having anti-inflammatory properties and regulating T cell polarization and cytokine production. However, whether IL-27 plays an important role in the acute stage of brain ischemia remains unclear. In the acute stage, IL-27 was upregulated after intracerebral ischemia in wild-type mice while mice lacking IL-27 showed decreased infarction area and suppressed inflammatory cytokines. These findings suggest that IL-27 may be involved in cerebral ischemia and could be a potential therapeutic target for mitigating inflammation and avoiding increasing the initial damage in cerebral ischemia.

摘要

缺血后炎症是脑缺血再灌注损伤进展中的一个重要步骤。细胞因子如白细胞介素17和23(IL-17、IL-23)已被证实与中风有关。IL-27是IL-12家族的成员,由IL-27p28和爱泼斯坦-巴尔病毒诱导基因3(EBI3)组成,具有抗炎特性并调节T细胞极化和细胞因子产生。然而,IL-27在脑缺血急性期是否起重要作用仍不清楚。在急性期,野生型小鼠脑缺血后IL-27上调,而缺乏IL-27的小鼠梗死面积减小且炎性细胞因子受到抑制。这些发现表明,IL-27可能参与脑缺血,并且可能是减轻炎症和避免增加脑缺血初期损伤的潜在治疗靶点。

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