Siahaan Andre Marolop Pangihutan, Ivander Alvin, Ginting Nicholas Rizki Banta, Bagus Pratama Muhammad Alfath, Silalahi Christine, Aries Tri Mulyani, Purba Michael Christian Martua
Department of Neurosurgery, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia.
Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia.
Korean J Neurotrauma. 2025 Jan 30;21(1):18-31. doi: 10.13004/kjnt.2025.21.e6. eCollection 2025 Jan.
Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Preclinical and clinical studies investigating the effects of curcumin on TBI indicate that curcumin can modulate essential signaling pathways and molecules that mediate neuroinflammation in TBI. This study aimed to explore the effects of turmeric on neuroinflammation and neurodegenerative disorder following repetitive traumatic brain injuries (rTBIs) in a rat model.
Sixty male were housed in a controlled environment. A modified Marmarou weight drop model was used. Turmeric extract was administered once daily in the morning. The avidin-biotin-peroxidase complex technique was used to evaluate the expression of all markers. Following incubation with normal rabbit serum, the slides were subsequently incubated with monoclonal antibodies targeting tau protein (AT-8), TAR DNA-binding protein 43 (TDP-43), glial fibrillary acidic protein (GFAP), and tumor necrosis factor (TNF)-α.
rTBI significantly increased the levels of inflammatory markers, such as TNF-α and GFAP. A substantial decrease of TNF-α expression was observed in the treatment group. A distinct trend was observed for GFAP expression, which was markedly decreased after the rest period compared to that in the trauma group. Phosphorylated tau expression decreased in both the treatment and pretreatment groups relative to that in the trauma and rest groups. TDP-43 expression was also significantly decreased in the treatment and pretreatment groups.
In conclusion, Turmeric demonstrates significant potential as a neuroprotective and anti-inflammatory agent in rTBI, especially when used as a preventive measure. Our findings challenge the significance of rest in concussion management.
创伤性脑损伤(TBI)是全球范围内导致死亡和残疾的主要原因。调查姜黄素对TBI影响的临床前和临床研究表明,姜黄素可调节介导TBI神经炎症的关键信号通路和分子。本研究旨在探讨姜黄对大鼠重复性创伤性脑损伤(rTBI)后神经炎症和神经退行性疾病的影响。
60只雄性大鼠饲养在可控环境中。采用改良的 Marmarou 重物坠落模型。姜黄提取物于每天上午给药一次。采用抗生物素蛋白-生物素-过氧化物酶复合物技术评估所有标志物的表达。用正常兔血清孵育后,玻片随后与靶向 tau 蛋白(AT-8)、TAR DNA 结合蛋白 43(TDP-43)、胶质纤维酸性蛋白(GFAP)和肿瘤坏死因子(TNF)-α 的单克隆抗体孵育。
rTBI显著增加了炎症标志物如TNF-α和GFAP的水平。在治疗组中观察到TNF-α表达大幅下降。观察到GFAP表达有明显趋势,与创伤组相比,休息期后GFAP表达明显下降。与创伤组和休息组相比,治疗组和预处理组中磷酸化tau表达均下降。治疗组和预处理组中TDP-43表达也显著下降。
总之,姜黄在rTBI中显示出作为神经保护和抗炎剂的显著潜力,尤其是用作预防措施时。我们的研究结果对脑震荡管理中休息的重要性提出了挑战。