BackgroundInhibiting secondary inflammatory damage caused by glial cells and creating a stable microenvironment is one of the main strategies to investigate drugs for the treatment of spinal cord injury. Acetyl‐11‐keto‐beta‐boswellic acid (AKBA) is the active component of the natural drug boswellia, which has anti‐inflammatory and antioxidant effects and offers a possible therapeutic option for spinal cord injury.MethodsIn this study, a spinal cord injury model was established by crushing spinal cord, respectively, to detect the M1 macrophage inflammatory markers: iNOS, TNF‐α, IL‐1β, and the M2 macrophage markers CD206, ARG‐1, IL‐10, and the detection of antioxidant enzymes and MDA. In vitro, macrophages were cultured to verify the main mechanism of the macrophage switch from Nrf2/HO‐1 to M2 type by flow cytometry, immunofluorescence, and other techniques. Macrophage and Schwann cell co‐culture validated the migration mechanism of Schwann cells promoted by AKBA.ResultsAKBA significantly enhanced the antioxidant enzyme activities of CAT, GSH‐Px, T‐AOC, and SOD, reduced MDA content, and reduced oxidative damage caused by spinal cord injury via the Nrf2/HO‐1 signaling pathway; AKBA mediates Nrf2/HO‐1/IL‐10, converts macrophages from M1 to M2 type, reduces inflammation, and promotes Schwann cell migration, thereby accelerating the repair of spinal cord injury in rats.ConclusionsOur work demonstrates that AKBA can attenuate oxidative stress as well as the secondary inflammatory injury caused by macrophages after SCI, promote Schwann cell migration to the injury site, and thus accelerate the repair of the injured spinal cord.

中文翻译：

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乙酰-11-酮-β-乳香酸调节巨噬细胞极化和雪旺细胞迁移，加速大鼠脊髓损伤修复


研究背景抑制胶质细胞引起的继发性炎症损伤、创造稳定的微环境是研究治疗脊髓损伤药物的主要策略之一。乙酰基-11-酮-β-乳香酸（AKBA）是天然药物乳香的活性成分，具有抗炎和抗氧化作用，为脊髓损伤提供了可能的治疗选择。通过粉碎脊髓建立模型，分别检测M1型巨噬细胞炎症标志物：iNOS、TNF-α、IL-1β，以及M2型巨噬细胞标志物CD206、ARG-1、IL-10，并检测抗氧化酶和丙二醛。体外培养巨噬细胞，通过流式细胞术、免疫荧光等技术验证巨噬细胞从Nrf2/HO-1向M2型转变的主要机制。巨噬细胞与雪旺细胞共培养验证了AKBA促进雪旺细胞迁移的机制。结果AKBA显着增强CAT、GSH-Px、T-AOC、SOD等抗氧化酶活性，降低MDA含量，减轻脊髓损伤造成的氧化损伤通过 Nrf2/HO-1 信号通路损伤脊髓； AKBA 介导 Nrf2/HO-1/IL-10，将巨噬细胞从 M1 型转化为 M2 型，减少炎症，促进雪旺细胞迁移，从而加速大鼠脊髓损伤的修复。结论我们的工作表明 AKBA 可以减轻氧化应激，如以及SCI后巨噬细胞引起的继发性炎症损伤，促进雪旺细胞向损伤部位迁移，从而加速损伤脊髓的修复。