Protective effects of bajijiasu in a rat model of Aβ₂₅₋₃₅-induced neurotoxicity

Abstract

Ethnopharmacological relevence: Neurodegenerative diseases (NDs) caused by neurons and/or myelin loss lead to devastating effects on patients׳ lives. Although the causes of such complex diseases have not yet been fully elucidated, oxidative stress, mitochondrial and energy metabolism dysfunction, excitotoxicity, inflammation, and apoptosis have been recognized as influential factors. Current therapies that were designed to address only a single target are unable to mitigate or prevent disease progression, and disease-modifying drugs are desperately needed, and Chinese herbs will be a good choice for screening the potential drugs. Previous studies have shown that bajijiasu, a dimeric fructose isolated from Morinda officinalis radix which was used frequently as a tonifying and replenishing natural herb medicine in traditional Chinese medicine clinic practice, can prevent ischemia-induced neuronal damage or death.

Materials and methods: In order to investigate whether bajijiasu protects against beta-amyloid (Aβ₂₅₋₃₅)-induced neurotoxicity in rats and explore the underlying mechanisms of bajijiasu in vivo, we prepared an Alzheimer׳s disease (AD) model by injecting Aβ25-35 into the bilateral CA1 region of rat hippocampus and treated a subset with oral bajijiasu. We observed the effects on learning and memory, antioxidant levels, energy metabolism, neurotransmitter levels, and neuronal apoptosis.

Results: Bajijiasu ameliorated Aβ-induced learning and memory dysfunction, enhanced antioxidative activity and energy metabolism, and attenuated cholinergic system damage. Our findings suggest that bajijiasu can enhance antioxidant capacity and prevent free radical damage. It can also enhance energy metabolism and monoamine neurotransmitter levels and inhibit neuronal apoptosis.

Conclusion: The results provide a scientific foundation for the use of Morinda officinalis and its constituents in the treatment of various AD. Future studies will assess the multi-target activity of the drug for the treatment of AD.

Keywords: Acetylcholine (PubChem CID: 187); Alzheimer׳s disease; Apoptosis; Bajijiasu; Beta-amyloid (PubChem CID: 3407255); Dopamine hydrochloride (PubChem CID: 65340); Malondialdehyde (PubChem CID: 10964); Mechanism; Neurotoxicity; Norepinephrine bitartrate (PubChem CID: 297812); Serotonin (PubChem CID: 5202).