Neuroprotective Effects of Berberine Chloride Against the Aluminium Chloride-Induced Alzheimer's Disease in Zebra Fish Larvae.

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease distinguished by cognitive and memory deficits. A lack of memory, cognition, and other forms of cognitive dissonance characterizes AD, which affects approximately 50 million people worldwide. This study aimed to identify the neuroprotective effects of berberine chloride (BC) against aluminium chloride (AlCl₃)-induced AD in zebrafish larvae by inhibiting oxidative stress and neuroinflammation. BC toxicity was assessed by evaluating survival rates, malformations, and heart rates in zebrafish larvae following treatment with varying concentrations of BC. This study elucidates the mechanisms of BC through an extensive range of biochemical assays, behavioral testing, and molecular docking analysis. The developmental toxicity assessment of BC indicated that doses up to 40 μM did not cause any developmental abnormalities until 96 h post fertilization. The LC₅₀ value of BC in zebrafish larvae was found to be 50.16 μM. The biochemical and behavioral changes induced by AlCl₃ in zebrafish larvae were significantly mitigated by BC treatment. Our findings demonstrate that BC can reduce total cholesterol and triglyceride levels in AlCl₃-induced AD zebrafish larvae. Our molecular docking results indicated that BC significantly interacted with the ABCA1 protein, suggesting that BC may act as an ABCA1 agonist. Based on our results, it can be concluded that BC may serve as an effective therapeutic agent for mitigating oxidative stress by altering cholesterol metabolism in AlCl₃-induced AD.