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首页> 外文期刊>Translational Stroke Research >The Splenic Response to Ischemic Stroke: What Have We Learned from Rodent Models?
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The Splenic Response to Ischemic Stroke: What Have We Learned from Rodent Models?

机译：脾对缺血性中风的反应：我们从啮齿类动物模型中学到了什么？

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The majority of promising experimental compounds have failed in clinical trials, highlighting the need for novel approaches to treat stroke. Much research has been devoted to elucidating the signaling pathways involved in delayed neuroinflammation that can be targeted at clinically relevant time points. The field of stroke research has benefited from experiments characterizing the temporal expression profiles of candidate cytokines, chemokines, matrix metalloproteinases, and other putative pro-inflammatory molecules. Yet, these data have offered only a glimpse into the complex pathological sequelae and have not advanced the treatment of neuropathies. Upon recognition that peripheral immune cell activation is involved in penumbral expansion, the spleen has emerged as a novel target that mediates the peripheral immune response and promotes pro-inflammatory injury. Although the precise mechanisms have yet to be elucidated, accumulated evidence demonstrates that focal cerebral ischemia alters cytokine, chemokine, and immune cell profiles in the spleen. Additionally, removal of this peripheral lymphoid organ is neuroprotective, and the efficacy of several protective therapies has been linked to actions at the level of the spleen. Future experiments aimed at identifying the splenic lymphocyte populations that respond to ischemic stroke, as well as their signaling mechanisms, are critical in developing novel therapies.
机译：大多数有希望的实验化合物在临床试验中均未通过，这凸显了对治疗中风的新颖方法的需求。已经进行了大量研究来阐明与神经炎性延迟有关的信号通路，这些信号通路可以针对临床相关的时间点。中风研究领域受益于表征候选细胞因子，趋化因子，基质金属蛋白酶和其他推定的促炎分子的时间表达特征的实验。然而，这些数据仅提供了对复杂病理后遗症的一瞥，并没有促进神经病的治疗。在认识到外周免疫细胞激活参与半影扩展后，脾脏已作为介导外周免疫反应并促进促炎性损伤的新靶标出现。尽管尚未阐明确切的机制，但是大量证据表明局灶性脑缺血会改变脾脏中的细胞因子，趋化因子和免疫细胞谱。另外，去除这种外周淋巴器官具有神经保护作用，并且几种保护性疗法的功效已与脾脏水平的作用联系在一起。旨在鉴定对缺血性中风有反应的脾淋巴细胞群及其信号传导机制的未来实验对开发新疗法至关重要。

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