神经炎症与阿尔茨海默病 (AD) 病理学密切相关，因此具有抗炎特性的补充剂可以帮助减缓 AD 的进展。本研究旨在评估口服脂质体封装的百里酚 (LET) 通过抗炎机制预防大鼠模型中阿尔茨海默病的潜在抗炎作用。将大鼠分为六组（每组 10 只）组），包括健康对照（Con）、阿尔茨海默病（AD）模型、用40和80mg/kg体重游离百里酚治疗的AD模型（TH40和TH80）、用40和80mg/kg LET治疗的AD模型体重（LET40 和 LET80）。潜伏期的行为反应（被动回避测试）、白细胞介素 1β (IL-1β)、白细胞介素 6 (IL-6)、肿瘤坏死因子 α (TNF-α) 和环氧合酶 2 (COX) 的浓度-2）和脑源性神经营养因子（BDNF）在血清和海马中进行评估。结果显示IL-1β（P=0.001）、IL-6（P=0.001）、TNF-α（P=0.001）浓度显着增加（ AD组与健康对照组大鼠相比，P=0.001）和COX-2（P=0.001）。 AD 诱导显着减少了步进延迟并揭示了被动回避性能的缺陷。结果还表明，游离百里酚（尤其是较高浓度）和 LTE 治疗可以降低 IL-1β（P<0.05）、IL-6（P<0.05）、TNF-α（P<0.05）和 COX 的血清浓度。与对照阿尔茨海默大鼠相比，海马和血清中BDNF增加-2（P<0.05）并增加BDNF（P<0.05）。血清和海马IL-1β浓度（r2=0.369，P=0.001）、IL-6（r2=0.386，P=0.001）、TNF-α（r2=0.412，P=0.001）、和COX-2（r2=0.357，P=0.001）。这意味着血清和海马的 IL-1β、IL-6、TNF-α 和 COX-2 浓度之间存在密切的正相关关系。LET 证明了其通过抑制 IL-1β、IL-1 来减轻 AD 模型中的神经炎症反应的能力。 6、TNF-α和COX-2指标。因此，它可以通过减少炎症反应来改善 AD 发病机制。版权所有 © 2024。由 Elsevier Inc. 出版。

Neuroinflammation is closely related to Alzheimer's Disease (AD) pathology, hence supplements with anti-inflammatory property could help attenuate the progression of AD. This study was conducted to evaluate the potential anti-inflammatory effects of liposome encapsulated thymol (LET), administered orally, in prevention of Alzheimer in a rat model by anti-inflammatory mechanisms.The rats were grouped into six groups (n = 10 animals per group), including Control healthy (Con), Alzheimer's disease (AD) model, AD model treated with free thymol in 40 and 80 mg/kg body weight (TH40 and TH80), AD model treated with LET in 40 and 80 mg/kg of body weight (LET40 and LET80). The behavioral response of step through latency (Passive Avoidance Test), concentrations of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) and brain-derived neurotrophic factor (BDNF) were assessed in serum and hippocampus.The results showed that significant increase in concentrations of IL-1β (P = 0.001), IL-6 (P = 0.001), TNF-α (P = 0.001) and COX-2 (P = 0.001) in AD group compared with healthy control rats. AD induction significantly reduced step through latency and revealed deficits in passive avoidance performance. The results also showed the treatment with free thymol especially in higher concentrations and also LTE could decrease serum concentrations of IL-1β (P < 0.05), IL-6 (P < 0.05), TNF-α (P < 0.05), and COX-2 (P < 0.05) and increase BDNF (P < 0.05) compared with control Alzheimer rats in hippocampus and serum. There were also significant correlations between serum and hippocampus concentrations of IL-1β (r2 = 0.369, P = 0.001), IL-6 (r2 = 0.386, P = 0.001), TNF-α (r2 = 0.412, P = 0.001), and COX-2 (r2 = 0.357, P = 0.001). It means a closed and positive relation between serum and hippocampus concentrations of IL-1β, IL-6, TNF-α, and COX-2.LET demonstrates its ability to attenuate neuroinflammatory reaction in AD model through suppression of IL-1β, IL-6, and TNF-α and COX-2 indicators. Hence, it can ameliorate AD pathogenesis by declining inflammatory reaction.Copyright © 2024. Published by Elsevier Inc.