Betanin mitigates scopolamine-induced cognitive impairment by restoring cholinergic function, boosting brain antioxidative status, and increasing BDNF level in the zebrafish model

Betalains obtained from Beta vulgaris (family Caryophyllales) are regularly consumed as part of the regular diet with medicinal benefits due to antioxidant and anti-inflammatory properties. The objective of this article was to evaluate betanin's neuroprotective properties in a scopolamine-induced zebrafish paradigm. Betanin (BET) (50, 100, and 200 mg/L), and donepezil (10 mg/L) were delivered to zebrafish in a treatment tank once a day for 8 days, while memory impairment was produced by scopolamine (100 mu M), which was given 60 min before behavioral assessments. The treatment dosages were determined based on acute toxicity studies. The existence of betacyanin and betaxanthins of BET was tested using liquid chromatography-mass spectrometry (LC-MS). The Y-maze task was used to examine the novelty and spatial memory, while the novel tank diving test was used to assess anxiety-like behavior (NTT). The activities of acetylcholinesterase (AChE) and the oxidative stress sensitivity in zebrafish brains were examined. Also, brain-derived neurotrophic factor (BDNF) level is quantified by an ELISA kit. Scopolamine-induced rises in AChE activity, memory loss, anxiety, and brain oxidant capacity were all reduced by BET. These results suggest that BET (50 and 100 mg/L) has a therapeutic ability to treat brain oxidative stress and cognitive deficits in amnesic zebrafish.

Automated summary

This study evaluated the neuroprotective properties of betanin obtained from Beta vulgaris in a scopolamine-induced zebrafish paradigm. The results showed that betanin could reduce memory impairment, anxiety, and brain oxidative stress caused by scopolamine, suggesting its therapeutic potential for cognitive deficits.