Based on the Dual Pathway of Interaction-Mediated NF-κB in Cell Apoptosis and Immune Inflammation to Study the Effect of Danzhi Xiaoyao Powder on the Learning and Cognitive Ability of AD Model Rats.

IF 3.2 Q3 CLINICAL NEUROLOGY
Degenerative neurological and neuromuscular disease Pub Date : 2025-04-14 eCollection Date: 2025-01-01 DOI:10.2147/DNND.S475290
Hu-Ping Wang, Ming-Cheng Li, Jiao Yang, Jun Zhou, Zhi-Peng Meng, Yun-Yun Hu, Yu-Jie Lyu, Yi-Qin Chen, Yu-Mei Han, Wen-Li Pei
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Abstract

Background: Apoptosis and immune inflammation play important roles in the pathological process of Alzheimer's disease (AD), but their specific pathogenesis is still unclear. Therefore, this article focuses on exploring the effects of Danzhi Xiaoyao Powder (DXP) on the learning and memory ability of AD model rats from the dual mechanisms of apoptosis and immune inflammation.

Methods: The AD model was replicated by injecting Okadaic acid (100 ng) into the bilateral hippocampus of rats. Successful rats were selected and orally administered with donepezil hydrochloride and DXP decoction for 42 days. Their learning and memory abilities, hippocampal morphology, Aβ expression, inflammatory factors, apoptotic factors, anti apoptotic factors, as well as the expression of pathway proteins and mRNA were detected.

Results: After DXP intervention, the learning and memory abilities of rats improved, the neuronal cell arrangement was more complete, the expression of Aβ decreased, the expression of pro-inflammatory cytokine and apoptotic factors decreased, the expression of anti apoptotic factors increased, Protein Kinase B (Akt) expression and activity significant up-regulation, and nuclear factor kappa-B (NF-κB), p38 MAPK (p38), MAPKAPK-2 (MK2), Cyclooxygenase-2 (COX-2) protein and mRNA expression were significantly down-regulated.

Conclusion: DXP can improve the learning and cognitive abilities of AD model rats, and its mechanism of action may be related to the regulation of the Akt/NF-κB apoptosis pathway mediated by NF-κB interaction and the p38MAPK/MK2/COX-2 immune inflammatory dual pathway.

基于相互作用介导的NF-κB参与细胞凋亡和免疫炎症的双通路研究丹栀逍遥散对AD模型大鼠学习认知能力的影响
背景:细胞凋亡和免疫炎症在阿尔茨海默病(AD)的病理过程中发挥重要作用,但其具体的发病机制尚不清楚。因此,本文重点从细胞凋亡和免疫炎症双重机制探讨丹栀逍遥散对AD模型大鼠学习记忆能力的影响。方法:采用大鼠双侧海马注射冈田酸(100 ng)复制AD模型。选取成功的大鼠,口服盐酸多奈哌齐和DXP汤42 d。检测大鼠学习记忆能力、海马形态、Aβ表达、炎症因子、凋亡因子、抗凋亡因子以及通路蛋白和mRNA的表达。结果:DXP干预后,大鼠学习记忆能力提高,神经元细胞排列更完整,Aβ表达减少,促炎细胞因子和凋亡因子表达减少,抗凋亡因子表达增加,蛋白激酶B (Akt)表达和活性显著上调,核因子κB (NF-κB)、p38 MAPK (p38)、MAPKAPK-2 (MK2)、环氧合酶-2 (COX-2)蛋白和mRNA表达显著下调。结论:DXP可提高AD模型大鼠的学习和认知能力,其作用机制可能与调节NF-κB相互作用介导的Akt/NF-κB凋亡通路和p38MAPK/MK2/COX-2免疫炎症双通路有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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