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首页> 外文期刊>The European Journal of Neuroscience >Reduction of rat brain CD8+ T-cells by levodopa/benserazide treatment after experimental stroke
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Reduction of rat brain CD8+ T-cells by levodopa/benserazide treatment after experimental stroke

机译：实验性中风后左旋多巴/苄丝肼治疗可减少大鼠脑CD8 + T细胞

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摘要

The activation of inflammatory cascades in the ischemic hemisphere impairs mechanisms of tissue reorganization with consequences for recovery of lost neurological function. Recruitment of T-cell populations to the post-ischemic brain occurs and represents a significant part of the inflammatory response. This study was conducted to investigate if treatment with levodopa, potentially acting as an immunomodulator, affects the T-cell accumulation in the post-ischemic brain. Male Sprague-Dawley rats were subjected to transient occlusion of the middle cerebral artery (tMCAO) for 105 min followed by levodopa/benserazide treatment (20 mg/kg/15 mg/kg) for 5 days initiated on day 2 post-stroke. One week after tMCAO, T-cell populations were analysed from brains, and levels of interleukin (IL)-1β, chemokine (C-X-C motif) ligand 1, IL-4, IL-5, interferon gamma and IL-13 were analysed. After levodopa/benserazide treatment, we found a significant reduction of cytotoxic T-cells (CD3+CD8+) in the ischemic hemisphere together with reduced levels of T-cell-associated cytokine IL-5, while other T-cell populations (CD3+, CD3+CD4+, CD3+CD4+CD25+) were unchanged compared with vehicle-treated rats. Moreover, a reduced number of cells was associated with reduced levels of intercellular adhesion molecule 1, expressed in endothelial cells, in the infarct core of levodopa/benserazide-treated animals. Together, we provide the first evidence that dopamine can act as a potential immunomodulator by attenuating inflammation in the post-ischemic brain.
机译：缺血性半球中炎症级联反应的激活削弱了组织重组的机制，并导致神经功能丧失的恢复。 T细胞群体向缺血后大脑的募集发生并且代表了炎症反应的重要部分。进行这项研究的目的是研究左旋多巴（可能起免疫调节剂的作用）是否会影响缺血后大脑中的T细胞积累。雄性Sprague-Dawley大鼠在中风后第二天开始接受大脑中动脉（tMCAO）的短暂闭塞105分钟，然后左旋多巴/苄丝肼治疗（20 mg / kg / 15 mg / kg）持续5天。 tMCAO一周后，从大脑中分析T细胞群，并分析白介素（IL）-1β，趋化因子（C-X-C基序）配体1，IL-4，IL-5，干扰素γ和IL-13的水平。左旋多巴/苄丝肼治疗后，我们发现缺血性半球中的细胞毒性T细胞（CD3 + CD8 +）显着减少，同时T细胞相关的细胞因子IL-5水平降低，而其他T细胞群体（CD3 +，CD3与载体治疗的大鼠相比，+ CD4 +，CD3 + CD4 + CD25 +）没有变化。此外，在左旋多巴/苄丝肼治疗的动物的梗塞核心中，细胞数量减少与内皮细胞中表达的细胞间粘附分子1水平降低有关。在一起，我们提供了第一个证据，即多巴胺可以通过减轻缺血后脑部的炎症来充当潜在的免疫调节剂。

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