Neuroinflammation plays a key role in the occurrence and development of neurodegenerative diseases. Microglia, the resident immune cells in the brain, have been recognized to contribute to neuroinflammation. Previous studies have shown that activated mast cells may be involved in surgery-induced neuroinflammation and neuronal apoptosis by using pharmacological methods. This study is aimed at ascertaining the exactly role of mast cells on neuroinflammation with the mast cell-deficient mice. Adult male C57BL6/J wild-type (WT) and mast cell-deficient (C57BL6/J KitWsh/Wsh (Wsh)) mice underwent tibial fracture surgery. Blood-brain barrier (BBB) breakdown, microglial activation, and neuroinflammatory levels were examined at 1 day after surgery. Surgery-induced BBB breakdown, microglial activation, and neuroinflammatory levels were significantly, pharmacologically reduced using a mast cell stabilizer, cromolyn sodium in WT mice (). These results were reproduced with mast cell deficiency. WT mice administered intraventricularly with cromolyn exhibited reduced BBB breakdown, microglial activation, and neuroinflammatory levels versus vehicle (). But there was no effect of cromolyn versus vehicle in Wsh mice, clarifying the specificity of cromolyn on brain mast cells. These findings demonstrated that activated mast cells promote surgery-induced BBB breakdown and neuroinflammation in mice, and open up a new therapeutic target for neuroinflammation-related diseases.

中文翻译：

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肥大细胞缺乏症可保护小鼠免于因手术引起的神经炎症。

神经炎症在神经退行性疾病的发生和发展中起关键作用。小胶质细胞是大脑中的固有免疫细胞，已被认为有助于神经炎症。先前的研究表明，通过使用药理学方法，活化的肥大细胞可能与手术诱导的神经炎症和神经元凋亡有关。这项研究旨在确定肥大细胞缺陷小鼠肥大细胞在神经炎症中的确切作用。成年雄性C57BL6 / J野生型（WT）和肥大细胞缺陷（C57BL6 / J KitWsh / Wsh（Wsh））小鼠进行了胫骨骨折手术。术后1天检查血脑屏障（BBB）分解，小胶质细胞活化和神经炎症水平。手术引起的血脑屏障分解，小胶质细胞活化和神经炎症水平显着，）。这些结果在肥大细胞缺乏的情况下得以再现。与媒介物相比，脑室内施用cromolyn的WT小鼠表现出降低的BBB分解，小胶质细胞活化和神经炎症水平（）。但是在Wsh小鼠中，克罗莫林对媒介物没有作用，这说明了克罗莫林对脑肥大细胞的特异性。这些发现表明，活化的肥大细胞可促进小鼠手术诱导的BBB分解和神经炎症，并为神经炎症相关疾病开辟了新的治疗靶标。