Ficus erecta Thunb. Leaves Ameliorate Cognitive Deficit and Neuronal Damage in a Mouse Model of Amyloid-β-Induced Alzheimer's Disease

• Published in: Frontiers in pharmacology 2021-04, Vol.12, p.607403-607403
• Main Authors: Sohn, Eunjin, Kim, Yu Jin, Kim, Joo-Hwan, Jeong, Soo-Jin
• Format: Article
• Language: English
• Subjects: Alzheimer’s disease; amyloid-β; Ficus erecta Thunb; neuroinflammation; neuronal loss; Pharmacology
• ISSN: 1663-9812; 1663-9812
• DOI: 10.3389/fphar.2021.607403

Alzheimer's disease (AD) pathogenesis is linked to amyloid plaque accumulation, neuronal loss, and brain inflammation. Thunb. is a food and medicinal plant used to treat inflammatory diseases. Here, we investigated the neuroprotective effects of Thunb. against cognitive deficit and neuronal damage in a mouse model of amyloid-β (Aβ)-induced AD. First, we confirmed the inhibitory effects of ethanol extracts of (EEFE) leaves on Aβ aggregation and . Next, behavioral tests (passive avoidance task and Morris water maze test) revealed EEFE markedly improved cognitive impairment in Aβ-injected mice. Furthermore, EEFE reduced neuronal loss and the expression of neuronal nuclei (NeuN), a neuronal marker, in brain tissues of Aβ-injected mice. EEFE significantly reversed Aβ-induced suppression of cAMP response element-binding protein (CREB) phosphorylation and brain-derived neurotrophic factor (BDNF) expression, indicating neuroprotection was mediated by the CREB/BDNF signaling. Moreover, EEFE significantly suppressed the inflammatory cytokines interleukin 1beta (IL-1β) and tumor necrosis factor alpha (TNF-α), and expression of ionized calcium-binding adaptor molecule 1 (Iba-1), a marker of microglial activation, in brain tissues of Aβ-injected mice, suggesting anti-neuroinflammatory effects. Taken together, EEFE protects against cognitive deficit and neuronal damage in AD-like mice via activation of the CREB/BDNF signaling and upregulation of the inflammatory cytokines.