Kandeel Mahmoud, Morsy Mohamed A, Abd El-Lateef Hany M, Marzok Mohamed, El-Beltagi Hossam S, Al Khodair Khalid M, Albokhadaim Ibrahim, Venugopala Katharigatta N
Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, Saudi Arabia.
Department of Pharmacology, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh, Egypt.
Front Pharmacol. 2023 Mar 9;14:1154607. doi: 10.3389/fphar.2023.1154607. eCollection 2023.
Alzheimer's disease (AD) is the most common type of dementia among older persons. This study looked at how Augmentin affected behavior, gene expression, and apoptosis in rats in which AD had been induced by scopolamine. The rats were divided into five groups: control, sham, memantine, Augmentin, and pre-Augmentin (the last group received Augmentin before scopolamine administration and was treated with memantine). A Morris water maze was utilized to measure spatial memory in the animals, and real-time quantitative reverse transcription PCR (qRT-PCR) and flow cytometry were employed to analyze gene expression and neuronal cell apoptosis, respectively. Memantine and Augmentin increased spatial memory in healthy rats. The use of scopolamine impaired spatial memory. Both Augmentin and memantine improved spatial memory in AD rats, particularly in the group that received memantine; however, the outcomes were more substantial when Augmentin was administered before scopolamine was given to induce AD. Furthermore, the expression of presenilin-2 (PSEN2) and inositol-trisphosphate 3-kinase B (ITPKB) increased, whereas the expression of DEAD-box helicase 5 (DDX5) fell in the AD-treated groups; however, the results were more substantial after combination therapy. According to flow cytometry studies, Augmentin pre-treatment reduced apoptosis in AD rats. The results showed that administering Augmentin to AD rats before memantine improved their spatial memory, reduced neuronal cell death, upregulated protective genes, and suppressed genes involved in AD pathogenesis.
阿尔茨海默病（AD）是老年人中最常见的痴呆类型。本研究观察了阿莫西林对东莨菪碱诱导AD的大鼠行为、基因表达和细胞凋亡的影响。大鼠分为五组：对照组、假手术组、美金刚组、阿莫西林组和预阿莫西林组（最后一组在给予东莨菪碱前接受阿莫西林治疗，并给予美金刚治疗）。利用莫里斯水迷宫测量动物的空间记忆，并分别采用实时定量逆转录PCR（qRT-PCR）和流式细胞术分析基因表达和神经元细胞凋亡。美金刚和阿莫西林可提高健康大鼠的空间记忆。东莨菪碱的使用损害了空间记忆。阿莫西林和美金刚均改善了AD大鼠的空间记忆，尤其是接受美金刚的组；然而，在给予东莨菪碱诱导AD之前给予阿莫西林时，结果更显著。此外，早老素-2（PSEN2）和肌醇三磷酸3激酶B（ITPKB）的表达增加，而DEAD盒解旋酶5（DDX5）的表达在AD治疗组中下降；然而，联合治疗后的结果更显著。根据流式细胞术研究，预治疗阿莫西林可减少AD大鼠的细胞凋亡。结果表明，在美金刚之前给AD大鼠服用阿莫西林可改善其空间记忆，减少神经元细胞死亡，上调保护基因，并抑制参与AD发病机制的基因。
