Kandeda Antoine Kavaye, Foutse Liliane Yimta, Tongoue Corneille, Djientcheu Jean Philippe, Dimo Théophile
Department of Animal Biology and Physiology, University of Yaoundé I, Yaoundé, Cameroon.
Department of Pharmacy, University of Montagnes, Bangangté, Cameroon.
Behav Neurol. 2025 Jan 6;2025:8815830. doi: 10.1155/bn/8815830. eCollection 2025.
Amnesia is a memory disorder marked by the inability to recall or acquire information. Hence, drugs that also target the neurogenesis process constitute a hope to discover a cure against memory disorders. This study is aimed at evaluating the antiamnesic and neurotrophic effects of the aqueous extract of () on in vivo and in vitro models of excitotoxicity. For the in vivo study, 42 adult male rats were divided into six groups of seven rats each and treated daily for 30 days as follows: normal control group (distilled water, 10 mL/kg, po), negative control group (distilled water, 10 mL/kg, po), positive control group (piracetam, 200 mg/kg, po), and 03 test groups (extract, 44, 88, and 176 mg/kg, po). Scopolamine (0.5 mg/kg, ip) was administered once daily, 45 min after these treatments, for 14 days, except in the normal control group. The animals were then subjected to short-term memory (new object recognition and T-maze) and long-term memory (radial arm maze) tests for 15 following days. Animals were then euthanized, and biochemical analyses (neurotransmitters, oxidative status, and neuroinflammation) were performed in the prefrontal cortex, hippocampus, and serum. Histological analysis of these organs was also carried out. In the in vitro study, the effect of the extract (5, 10, 19, 40, 77, 153, 306, 615, 1225, and 2450 g/mL) was assessed on the viability of primary cortical neurons exposed to L-glutamate (0.1 mg/mL). Scopolamine induced memory impairment and increased oxidative stress, neuroinflammation, and neuronal loss. extract (44 mg/kg) reduced ( < 0.001) short- and long-term memory deficit. It also increased ( < 0.01) the concentration of acetylcholine, reduced ( < 0.001) that of malondialdehyde, and limited ( < 0.001) neuroinflammation and neuronal loss ( < 0.001). In addition, the extract (2450 g/mL) increased ( < 0.001) the percentage of viable cells. These results suggest that the extract has effects on amnesia and neurogenesis. These effects seem to be mediated by antioxidant and anti-inflammatory modulations.
失忆症是一种记忆障碍，其特征是无法回忆或获取信息。因此，针对神经发生过程的药物为发现治疗记忆障碍的方法带来了希望。本研究旨在评估（）水提取物对兴奋性毒性的体内和体外模型的抗失忆和神经营养作用。在体内研究中，将42只成年雄性大鼠分为六组，每组七只，每天进行如下处理，持续30天：正常对照组（蒸馏水，10 mL/kg，口服）、阴性对照组（蒸馏水，10 mL/kg，口服）、阳性对照组（吡拉西坦，200 mg/kg，口服）以及三个试验组（提取物，44、88和176 mg/kg，口服）。除正常对照组外，每天在这些处理45分钟后腹腔注射东莨菪碱（0.5 mg/kg），持续14天。然后在接下来的15天对动物进行短期记忆（新物体识别和T迷宫）和长期记忆（放射状臂迷宫）测试。之后对动物实施安乐死，并在前额叶皮质、海马体和血清中进行生化分析（神经递质、氧化状态和神经炎症）。还对这些器官进行了组织学分析。在体外研究中，评估了提取物（5、10、19、40、77、153、306、615、1225和2450 μg/mL）对暴露于L-谷氨酸（0.1 mg/mL）的原代皮质神经元活力的影响。东莨菪碱导致记忆障碍，并增加氧化应激、神经炎症和神经元损失。提取物（44 mg/kg）减轻了（P<0.001）短期和长期记忆缺陷。它还增加了（P<0.01）乙酰胆碱浓度，降低了（P<0.001）丙二醛浓度，并限制了（P<0.001）神经炎症和神经元损失（P<0.001）。此外，提取物（2450 μg/mL）增加了（P<0.001）活细胞百分比。这些结果表明该提取物对失忆症和神经发生有作用。这些作用似乎是由抗氧化和抗炎调节介导的。
