Cognitive decline is one of the most obvious symptoms of traumatic brain injury (TBI). Previous studies have demonstrated that cognitive decline is related to substantially increased neuroinflammation and decreased neurogenesis in the hippocampus in a rat model of TBI. Using this model, we explored the role of curcumin (Cur) in ameliorating TBI-impaired spatial memory because Cur has been shown to exhibit anti-chronic-neuroinflammatory, neurogenesis-promoting, and memory-improving properties.

Animals received daily Cur or vehicle treatment for 28 days after TBI and also received 50-bromodeoxyuridine(BrdU) for the first 7 days of the treatment for assaying neurogenesis. An optimal Cur dose of 30 mg/kg, selected from a range of 10–50 mg/kg, was used for the present study. Neuroinflammation was evaluated by astrocyte hypertrophy, activated microglia, and inflammatory factors in the hippocampus. Behavioral water-maze studies were conducted for 5 days, starting at 35-day post-TBI. The tropomyosin receptor kinase B (Trkb) inhibitor, ANA-12, was used to test the role of the brain-derived neurotrophic factor (BDNF)/ TrkB/Phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in regulating inflammation and neurogenesis in the hippocampus.

Treatment with Cur ameliorated the spatial memory of TBI rats, reduced TBI-induced chronic inflammation, typified by diminished astrocyte hypertrophy, reduction in activated microglia, declined inflammatory factors, and increased neurogenesis in the hippocampus. We also found that BDNF/Trkb/PI3K/Akt signaling was involved in the effects of Cur in TBI rats.

Thus, Cur treatment can ameliorate the spatial memory in a murine model of TBI, which may be attributable to decreased chronic neuroinflammation, increased hippocampal neurogenesis, and/or BDNF/Trkb/PI3K/Akt signaling.

认知能力下降是外伤性脑损伤 (TBI) 最明显的症状之一。先前的研究表明，认知能力下降与 TBI 大鼠模型中海马神经炎症显着增加和神经发生减少有关。使用该模型，我们探索了姜黄素 (Cur) 在改善 TBI 受损空间记忆中的作用，因为 Cur 已被证明具有抗慢性神经炎症、促进神经发生和改善记忆的特性。

动物在 TBI 后接受每日 Cur 或载体治疗 28 天，还在治疗的前 7 天接受 50-溴脱氧尿苷 (BrdU) 以检测神经发生。本研究使用从 10–50 mg/kg 范围中选择的 30 mg/kg 的最佳 Cur 剂量。通过星形胶质细胞肥大、激活的小胶质细胞和海马中的炎症因子来评估神经炎症。从 TBI 后 35 天开始，进行了 5 天的行为水迷宫研究。原肌球蛋白受体激酶 B (Trkb) 抑制剂 ANA-12 用于测试脑源性神经营养因子 (BDNF)/TrkB/磷酸肌醇 3-激酶 (PI3K)/Akt 信号通路在调节炎症和神经发生中的作用海马体。

Cur 治疗改善了 TBI 大鼠的空间记忆，减少了 TBI 诱导的慢性炎症，以星形胶质细胞肥大减少、活化小胶质细胞减少、炎症因子减少和海马神经发生增加为代表。我们还发现 BDNF/Trkb/PI3K/Akt 信号与 Cur 在 TBI 大鼠中的作用有关。

因此，Cur 治疗可以改善 TBI 小鼠模型的空间记忆，这可能归因于慢性神经炎症减少、海马神经发生增加和/或 BDNF/Trkb/PI3K/Akt 信号传导。