Amenotie Akhator J, Ben-Azu Benneth, Esuku Daniel T, Chijioke Bienose S, Abo Ekpekuro, Ozah Esther O, Lawrence Ewhre O, Efejene Ofejiro I, Onyeukwu Onyeka B, Alabi Babatunde A, Ajayi Abayomi M
DELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Basic Medical Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Delta State University, Abraka, Delta State, Nigeria.
Neurotox Res. 2025 Jun 5;43(3):26. doi: 10.1007/s12640-025-00750-6.
Memory decline is a common hallmark signal of neurodegenerative diseases marked by elevated neuroinflammatory cytokines, oxidative damage and cholinergic insufficiency in cortical regions. Studies indicate that inhibiting these cytokines and associated markers may enhance memory and provide neuroprotection. This study investigates the effects of sabinene, a neuroprotective monoterpene found in essential oils with neuroprotective and antioxidant properties, on lipopolysaccharide (LPS)-induced neuroinflammation, oxidative stress and learning/memory impairment in mice. In this study, mice in groups 1 and 2 received normal saline, while groups 3-5 were pretreated with sabinene (5, 10, and 20 mg/kg). Group 6 received donepezil (1 mg/kg) orally. Groups 2-6 were additionally injected with LPS (0.5 mg/kg, i.p.) 30 min post-treatment for 7 days. Behavioral consequences indicating spatial and non-spatial deficits were assessed through Y-maze and novel-object recognition tests, along with locomotor functions conducted. Biochemical markers of neuroinflammation (TNF-α, IL-6), oxidative stress (glutathione, peroxidase, malondialdehyde, nitrite), cholinergic function, and molybdenum enzymes were analyzed in the prefrontal-cortex (PFC) and hippocampus. Sabinene treatment mitigated LPS-induced memory impairments and reduced motor activity. It also significantly decreased acetylcholinesterase activity and malondialdehyde levels in the hippocampus and PFC while increasing glutathione and glutathione peroxidase levels, respectively. Moreover, sabinene reduced LPS-induced molybdenum enzyme elevation in the PFC. Compared to LPS, sabinene significantly lowered TNF-α and IL-6 levels in the PFC and hippocampus while protecting neuronal cell damage in the PFC. Overall, sabinene enhances memory function in LPS-treated mice by reducing oxidative stress and neuroinflammation while improving cholinergic activity and molybdenum enzymes in the cortical regions of mice brains.
记忆衰退是神经退行性疾病的常见标志性信号，其特征是神经炎症细胞因子升高、氧化损伤以及皮质区域胆碱能不足。研究表明，抑制这些细胞因子和相关标志物可能会增强记忆力并提供神经保护作用。本研究调查了桧烯（一种存在于具有神经保护和抗氧化特性的香精油中的神经保护单萜）对脂多糖（LPS）诱导的小鼠神经炎症、氧化应激和学习/记忆损伤的影响。在本研究中，第1组和第2组小鼠接受生理盐水，而第3 - 5组用桧烯（5、10和20毫克/千克）进行预处理。第6组口服多奈哌齐（1毫克/千克）。第2 - 6组在治疗后30分钟额外注射LPS（0.5毫克/千克，腹腔注射），持续7天。通过Y迷宫和新物体识别测试评估表明空间和非空间缺陷的行为后果，同时进行运动功能测试。在额叶前皮质（PFC）和海马体中分析神经炎症（TNF-α、IL-6）、氧化应激（谷胱甘肽、过氧化物酶、丙二醛、亚硝酸盐）、胆碱能功能和钼酶的生化标志物。桧烯治疗减轻了LPS诱导的记忆损伤并降低了运动活性。它还分别显著降低了海马体和PFC中的乙酰胆碱酯酶活性和丙二醛水平，同时提高了谷胱甘肽和谷胱甘肽过氧化物酶水平。此外，桧烯降低了LPS诱导的PFC中钼酶的升高。与LPS相比，桧烯显著降低了PFC和海马体中的TNF-α和IL-6水平，同时保护了PFC中的神经元细胞损伤。总体而言，桧烯通过减少氧化应激和神经炎症，同时改善小鼠大脑皮质区域的胆碱能活性和钼酶，增强了LPS处理小鼠的记忆功能。
