Authors: Tian, Ji-Sha | Zhai, Qi-Jin | Zhao, Ying | Chen, Rui | Zhao, Lian-Dong
Article Type:
Research Article
Abstract:
Alzheimer’s Disease (AD) is one of the commonest neural degenerations in an aging population, and has become a global health challenge. 2-(2-benzofuranyl)-2-imidazoline (2-BFI) was reported to effectively improve the neural damage of patients with neuropathological disorders. In the present study, we investigated the effect of 2-BFI on the improvement of antioxidative, inflammation, and apoptosis in AD rats. Sprague-Dawley rats (2 months old, n = 40 ) were used in this study and after injection of A β 1 - 42 into hippocampal CA1 (Cornu Ammonis) region, the rats were given high, moderate
…and low dose of 2-BFI though intraperitoneal (i.p.) injection. Then spatial memory and navigation ability were analyzed by Morris water maze. For molecular testing, chemical colorimetry, ELISA and immunoblotting were performed to measure the activities of antioxidative enzymes, the abundance of immune cytokines and expression of apoptotic proteins, respectively. Hematoxylin and Eosin staining were used to analyze the pathological changes. We observed that 2-BFI significantly ameliorated the learning and memory abilities in rat models with AD by dosage treatment, as demonstrated by the shortened learning latency and greater times of travel across the platform quadrant. Additionally, reactive oxygen species (ROS) and malondialdehyde (MDA), were decreased after treatment on 2-BFI with dosage dependency, while the activities of superoxidase dismutase (SOD) and (GPX) glutathione peroxidase were in turn enhanced, suggesting that 2-BFI could protect the antioxidative enzymes and reduce oxidative stress in the hippocampus. Moreover, the expression of inflammatory factors including TNF-a and IL-1 β were decreased after 2-BFI treatment. Additionally, neuronal apoptosis was also attenuated, as shown by Western blot results. Taken together, the cognitive impairment in AD rats could be significantly improved by 2-BFI in a dose-dependent manner through suppressing oxidant accumulation, inhibition of inflammatory response, thus enhancing neural viability.
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Keywords: Alzheimer’s disease, 2-BFI, ROS, inflammatory, apoptosis
DOI: 10.3233/JIN-170032
Citation: Journal of Integrative Neuroscience,
vol. 16, no. 4, pp. 385-400, 2017
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