Background: Neuroinflammation subsequent to traumatic brain injury (TBI) is important for the recovery of patients and is associated with neurodegenerative changes post-TBI. The tripartite motif containing 44 (TRIM44) protein is an E3 ligase involved in the regulation of immune function with no previously known link to TBI. This study explores the connection between TRIM44 and TBI. Methods: After induction of TBI in rats by control cortex injury, TRIM44 expressions were determined with quantitative real-time reverse transcription polymerase chain reaction and Western blot, and Toll-like receptor 4 (TLR4)-NF-κB signaling was examined by the expression of TLR4, p65 phosphorylation, and the specific NF-κB transcription activity. The effects of TRIM44 knockdown on inflammation, neurological function, and TLR4-NF-κB signaling in TBI rats were revealed by the detection of proinflammatory cytokines and TLR4-NF-κB signaling molecules, modified neurological severity score, brain water content, and Evans blue permeability. Results: We found that TRIM44 expression was significantly increased following TBI induction along with TLR4-NF-κB activation. Silencing of TRIM44 suppressed proinflammatory cytokine production, improved neurological outcomes, alleviated brain edema, and inhibited TLR4-NF-κB signaling in TBI rats. Conclusion: Our findings suggest that suppressing TRIM44 or modulation of relevant pathways may be a therapeutic strategy for TBI.
Neuroimmunomodulation

中文翻译：

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TRIM44 的沉默通过下调 TLR4-NF-κB 信号传导抑制炎症并减轻大鼠创伤性脑损伤

背景：创伤性脑损伤 (TBI) 后的神经炎症对患者的康复很重要，并且与 TBI 后的神经退行性变化有关。包含 44 (TRIM44) 蛋白的三联基序是一种 E3 连接酶，参与免疫功能的调节，与 TBI 没有以前已知的联系。本研究探讨了 TRIM44 和 TBI 之间的联系。方法：通过对照皮质损伤诱导大鼠 TBI 后，通过定量实时逆转录聚合酶链反应和蛋白质印迹测定 TRIM44 表达，并通过 TLR4 的表达检测 Toll 样受体 4 (TLR4)-NF-κB 信号传导、p65 磷酸化和特定的 NF-κB 转录活性。通过检测促炎细胞因子和 TLR4-NF-κB 信号分子、改良神经严重程度评分、脑含水量和伊文思蓝，揭示了 TRIM44 敲低对 TBI 大鼠炎症、神经功能和 TLR4-NF-κB 信号的影响渗透性。结果：我们发现 TBI 诱导后 TRIM44 表达显着增加以及 TLR4-NF-κB 激活。TRIM44 的沉默抑制了 TBI 大鼠的促炎细胞因子产生，改善了神经系统结果，减轻了脑水肿，并抑制了 TLR4-NF-κB 信号传导。结论：我们的研究结果表明，抑制 TRIM44 或调节相关通路可能是 TBI 的治疗策略。
神经免疫调节