Abstract
Alzheimer’s disease (AD) pathogenesis is linked to amyloid plaque accumulation, neuronal loss, and brain inflammation. Ficus erecta Thunb. is a food and medicinal plant used to treat inflammatory diseases. Here, we investigated the neuroprotective effects of F. erecta 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 F. erecta (EEFE) leaves on Aβ aggregation in vivo and in vitro. 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.
Highlights
Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disorder that leads to memory loss and learning deficit
One-way analysis of variance (ANOVA) revealed the significance between group effects Figures 5E,F (NOR, Aβ, ethanol extracts of F. erecta (EEFE)-50, EEFE-150, M-10; F (4, 10) 11.46, p 0.0009 of hippocampus and F (4, 10) 6.159, p 0.009 of cortex)
We explored for the first time the pharmacological effects of F. erecta leaves in AD or ADrelated diseases
Summary
Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disorder that leads to memory loss and learning deficit. The main trademark of AD pathology is amyloid-β (Aβ) peptide accumulation and the large aggregates (plaques) formation in the brain (Longo and Massa, 2004; Morroni et al, 2018). Prevention of Aβ aggregation and accumulation is a potential strategy for the treatment of AD. Anti-Aβ treatment has failed in clinical trials, Aβ is still considered a key target molecule for developing novel AD therapies (Lim et al, 2019; Sikanyika et al, 2019). Anti-Alzheimer’s disease of Ficus erecta severe side effects. In the face of these limitations, complementary and alternative therapies could offer a solution to block the progression of AD
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