Ischemic stroke leads to severe neurological dysfunction in adults. Hyperbaric oxygen (HBO) induces tolerance to cReperfusion inj/reperfusion (I/R) injury. Therefore, our aims were to investigate whether SIRT1 participates in regulatingin the neuro-protective effect of HBO in a cerebral I/R model and its mechanism. Mice N2a cells were used to construct an oxygen deprivation/reperfusion (OGD/R) model to simulate in vitro brain I/R injury and to evaluate the role of HBO in OGD/R stimulated cells. Cell proliferation was detected using MTT, and apoptosis was determined by flow cytometry. ELISA was used to measure the concentration of TNF-α, IL-1β and IL-6 related inflammatory factors. RT-qPCR and western blot assays were performed to test the expression of SIRT1. Immunoprecipitation was used to detect acetylation of HMGB1. Expression of SIRT1 was obviously reduced after OGD/R treatment in N2a cells, while SIRT1 was obviously enhanced in HBO treated cells. Moreover, knockdown of SIRT1 induced neuro-inflammation damage in cells and HBO effectively improved the inflammatory response in OGD/R treated cells by affecting SIRT1 levels. Furthermore, HBO induced the deacetylation of HMGB1 via regulating SIRT1. Interestingly, HBO via regulating the SIRT1-induced HMGB1 deacetylation and suppressing MMP-9 improved ischemic brain injury. HBO regulated ischemic brain injury via regulation of SIRT1-induced HMGB1 deacetylation, making it a potential treatment for ischemic brain injury treatment.

中文翻译：

---

高压氧通过介导 SIRT1 诱导的 HMGB1 去乙酰化改善 cReperfusion inj/再灌注损伤

缺血性中风导致成人严重的神经功能障碍。高压氧 (HBO) 诱导对 cReperfusion 注射/再灌注 (I/R) 损伤的耐受性。因此，我们的目的是研究SIRT1是否参与调节HBO在脑I/R模型中的神经保护作用及其机制。使用小鼠 N2a 细胞构建缺氧/再灌注 (OGD/R) 模型以模拟体外脑 I/R 损伤并评估 HBO 在 OGD/R 刺激细胞中的作用。MTT检测细胞增殖，流式细胞术检测细胞凋亡。采用ELISA法测定TNF-α、IL-1β和IL-6相关炎症因子的浓度。进行 RT-qPCR 和蛋白质印迹分析以测试 SIRT1 的表达。免疫沉淀用于检测HMGB1的乙酰化。OGD/R处理后N2a细胞中SIRT1的表达明显降低，而HBO处理的细胞中SIRT1的表达明显增强。此外，敲低 SIRT1 诱导细胞神经炎症损伤，HBO 通过影响 SIRT1 水平有效改善 OGD/R 处理细胞的炎症反应。此外，HBO 通过调节 SIRT1 诱导 HMGB1 去乙酰化。有趣的是，HBO 通过调节 SIRT1 诱导的 HMGB1 去乙酰化和抑制 MMP-9 改善了缺血性脑损伤。HBO 通过调节 SIRT1 诱导的 HMGB1 去乙酰化来调节缺血性脑损伤，使其成为治疗缺血性脑损伤的潜在疗法。抑制 SIRT1 诱导细胞神经炎症损伤，HBO 通过影响 SIRT1 水平有效改善 OGD/R 处理细胞的炎症反应。此外，HBO 通过调节 SIRT1 诱导 HMGB1 去乙酰化。有趣的是，HBO 通过调节 SIRT1 诱导的 HMGB1 去乙酰化和抑制 MMP-9 改善了缺血性脑损伤。HBO 通过调节 SIRT1 诱导的 HMGB1 去乙酰化来调节缺血性脑损伤，使其成为治疗缺血性脑损伤的潜在疗法。抑制 SIRT1 诱导细胞神经炎症损伤，HBO 通过影响 SIRT1 水平有效改善 OGD/R 处理细胞的炎症反应。此外，HBO 通过调节 SIRT1 诱导 HMGB1 去乙酰化。有趣的是，HBO 通过调节 SIRT1 诱导的 HMGB1 去乙酰化和抑制 MMP-9 改善了缺血性脑损伤。HBO 通过调节 SIRT1 诱导的 HMGB1 去乙酰化来调节缺血性脑损伤，使其成为治疗缺血性脑损伤的潜在疗法。