脾脏通过干扰素 γ 信号导致中风引起的神经退行性变。
The spleen contributes to stroke induced neurodegeneration through interferon gamma signaling.
机构信息
Department of Molecular Pharmacology and Physiology, School of Basic Biomedical Sciences, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
出版信息
Metab Brain Dis. 2012 Jun;27(2):131-41. doi: 10.1007/s11011-012-9283-0. Epub 2012 Feb 22.
Abstract
Delayed neuronal death associated with stroke has been increasingly linked to the immune response to the injury. Splenectomy prior to middle cerebral artery occlusion (MCAO) is neuroprotective and significantly reduces neuroinflammation. The present study investigated whether splenic signaling occurs through interferon gamma (IFNγ). IFNγ was elevated early in spleens but later in the brains of rats following MCAO. Splenectomy decreased the amount of IFNγ in the infarct post-MCAO. Systemic administration of recombinant IFNγ abolished the protective effects of splenectomy with a concurrent increase in INFγ expression in the brain. These results suggest a role for spleen-derived IFNγ in stroke pathology.
摘要
与中风相关的迟发性神经元死亡与对损伤的免疫反应越来越相关。大脑中动脉闭塞（MCAO）前的脾切除术具有神经保护作用，并能显著减轻神经炎症。本研究探讨了脾信号是否通过干扰素γ（IFNγ）发生。MCAO 后，大鼠脾脏中的 IFNγ 早期升高，但随后在大脑中升高。脾切除术减少了 MCAO 后梗死灶中 IFNγ 的含量。重组 IFNγ 的全身给药消除了脾切除术的保护作用，同时大脑中 IFNγ 的表达增加。这些结果表明，脾源性 IFNγ 在中风发病机制中起作用。
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