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Updated: May 11, 2026

Strategies for Study of Neuroprotection from Cold-preconditioning
Published on: September 2, 2010
Interleukin-27 deletion has neuroprotective effects in the acute ischemic stage of cerebral infarction
Takashi Furukawa1, Yasunobu Miyake2, Hiroshi Ito3
1Department 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.
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.
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