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

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Abstract

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 µM), 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.

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Data availability

The datasets generated during and/or analyzed during the current study are available from the corresponding author upon reasonable request.

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Acknowledgements

I would like to thank SPPSPTM, SVKM’s NMIMS University, Mumbai, for their support.

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Authors and Affiliations

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Contributions

Conceptualization, GK and BT; methodology, GK and BT; software, BT; investigation, BT; writing—original draft preparation, BT; writing, review, and editing, GK; supervision, GK; All the authors read and approved the final manuscript.

Corresponding author

Correspondence to Ginpreet Kaur.

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Ethics approval

The Institutional Animal Ethics Committee permitted the study protocol (approval no. CPCSEA/IAEC/P-18/2019 dated March 22, 2019), which was formed following the guidelines of the Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA), Government of India, and The National Institutes of Health (NIH) guidelines for the care of experimental animals were followed.

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Conflict of interest

The authors declare no competing interests.

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Highlights

• Betanin ameliorates cognitive dysfunction in a scopolamine-induced zebrafish model.

• In a novel tank test, betanin improves exploratory behavior.

• Betanin promotes zebrafish novelty response and spatial memory in the Y maze test.

• Betanin significantly decreases AChE-specific activity.

• In zebrafish, betanin therapy dramatically increases the antioxidant state of the brain.

• Betanin treatment raises BDNF levels in the brain of zebrafish.

• Betanin (50 and 100 mg/L) showed promising cognitive-enhancing potential.

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Supplementary file1 (DOCX 47 KB)

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Thawkar, B.S., Kaur, G. Betanin mitigates scopolamine-induced cognitive impairment by restoring cholinergic function, boosting brain antioxidative status, and increasing BDNF level in the zebrafish model. Fish Physiol Biochem 49, 335–349 (2023). https://doi.org/10.1007/s10695-023-01185-6

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  • DOI: https://doi.org/10.1007/s10695-023-01185-6

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