Microglia, as the first line of defence of the central nervous system (CNS), has a major role in inflammatory response. It was reported that isoflurane has a neuroprotective role in the pathological process of CNS by interfering with inflammatory response. While the mechanism and function of isoflurane in microglia-mediated inflammation are still not clearly articulated. In our study, the inflammation model was established by the activation of lipopolysaccharide (LPS) in BV2 cells in vitro. The results demonstrated that isoflurane inhibited the release of nitric oxide (NO) and enhanced the survival of BV2 cells, meanwhile, isoflurane reduced the levels of inflammatory factors and downregulated the expressions of inflammation-related genes and proteins in LPS-mediated BV2 cells. Furthermore, we demonstrated that overexpression of high-mobility group box 1 protein (HMGB1) could reverse the reduction in NO concentration, enhancement of cell BV2 viability and inhibition of inflammatory response, which were mediated by isoflurane in LPS-induced BV2 cells. Therefore, we suggested that isoflurane inhibits the activation of LPS-induced neuro microglia and reduces the release of inflammatory factors by regulating HMGB1, suggesting that isoflurane might play a protective role in LPS-induced neuroinflammation through the HMGB1 pathway.

中文翻译：

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异氟烷通过调节HMGB1 / TLRs途径对脂多糖诱导的BV2小胶质细胞神经炎的神经保护作用。

小胶质细胞作为中枢神经系统（CNS）的第一道防线，在炎症反应中起主要作用。据报道，异氟烷通过干扰炎症反应而在中枢神经系统的病理过程中具有神经保护作用。虽然异氟醚在小胶质细胞介导的炎症中的机制和功能尚不清楚。在我们的研究中，炎症模型是通过体外BV2细胞中脂多糖（LPS）的激活而建立的。结果表明，异氟醚抑制一氧化氮（NO）的释放并提高BV2细胞的存活率，同时，异氟烷降低了LPS介导的BV2细胞中的炎症因子水平，并下调了炎症相关基因和蛋白的表达。此外，我们证明过表达高迁移率的第1族框蛋白（HMGB1）可以逆转LPS诱导的BV2细胞中异氟烷介导的NO浓度降低，细胞BV2活力增强和炎症反应抑制。因此，我们建议异氟烷通过调节HMGB1来抑制LPS诱导的神经小胶质细胞的激活并减少炎症因子的释放，这表明异氟烷可能通过HMGB1途径在LPS诱导的神经炎症中起保护作用。