This preprint is under consideration at Metabolic Brain Disease. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Research Article
Wachiryah Thong-asa
Animal Toxicology and Physiology Specialty Research Unint
Corresponding Author
ORCiD: https://orcid.org/0000-0003-0065-7339
License:
This work is licensed under a CC BY 4.0 License. Read Full License
The present study aimed to investigate betanin’s neuroprotective effect in mice with rotenone-induced Parkinson-like motor dysfunction and neurodegeneration. Forty male ICR mice were divided into 4 groups: Sham-veh, Rot-veh, Rot-Bet100 and Rot-Bet200. Rotenone (Rot) at 2.5 mg/kg/48 h was subcutaneous injected, and betanin (Bet) at 100 and 200 mg/kg/48 h were given alternately with the Rot injections in Rot-Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), neuronal degeneration in the motor cortex (MC), striatum (Str) and substantia nigra par compacta (SNc) were evaluated. The immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in SNc were also measured. We found that rotenone significantly decreased the time to fall in a hanging wire test after the 4th week and after the rotarod test at the 6th week (p<0.05). The percentage of neuronal degeneration in MC, Str and SNc (p<0.05) significantly increased, and the TH density in Str and in SNc (p<0.05) significantly decreased. Betanin at 100 and 200 mg/kg significantly prevented MC, Str and SNc neuronal degeneration (p<0.05) and prevented the decrease of TH density in Str and in SNc (p<0.05). These findings appeared concurrently with improved effects on the time to fall in hanging wire and rotarod tests (p<0.05). Treatment with betanin significantly prevented increased MDA levels and boosted GSH, CAT and SOD activities (p<0.05). Betanin exhibits neuroprotective effects against rotenone-induced Parkinson in mice regarding both motor dysfunction and neurodegeneration. Betanin’s neurohealth benefit relates to its powerful antioxidative property. Therefore, betanin use in neurodegenerative disease therapy is interesting to study.
Keywords
Betanin, motor cortex, motor dysfunction, Parkinson disease, striatum, substantia nigra
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This preprint is under consideration at Metabolic Brain Disease. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Wachiryah Thong-asa
Animal Toxicology and Physiology Specialty Research Unint
Corresponding Author
ORCiD: https://orcid.org/0000-0003-0065-7339
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 23 Apr, 2021
No community comments so far
Reviews received
Received 20 Apr, 2021
Reviewers invited
Invitations sent on 19 Apr, 2021
First submitted
On 08 Apr, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Head & Neck Surgery
License:
This work is licensed under a CC BY 4.0 License. Read Full License
The present study aimed to investigate betanin’s neuroprotective effect in mice with rotenone-induced Parkinson-like motor dysfunction and neurodegeneration. Forty male ICR mice were divided into 4 groups: Sham-veh, Rot-veh, Rot-Bet100 and Rot-Bet200. Rotenone (Rot) at 2.5 mg/kg/48 h was subcutaneous injected, and betanin (Bet) at 100 and 200 mg/kg/48 h were given alternately with the Rot injections in Rot-Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), neuronal degeneration in the motor cortex (MC), striatum (Str) and substantia nigra par compacta (SNc) were evaluated. The immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in SNc were also measured. We found that rotenone significantly decreased the time to fall in a hanging wire test after the 4th week and after the rotarod test at the 6th week (p<0.05). The percentage of neuronal degeneration in MC, Str and SNc (p<0.05) significantly increased, and the TH density in Str and in SNc (p<0.05) significantly decreased. Betanin at 100 and 200 mg/kg significantly prevented MC, Str and SNc neuronal degeneration (p<0.05) and prevented the decrease of TH density in Str and in SNc (p<0.05). These findings appeared concurrently with improved effects on the time to fall in hanging wire and rotarod tests (p<0.05). Treatment with betanin significantly prevented increased MDA levels and boosted GSH, CAT and SOD activities (p<0.05). Betanin exhibits neuroprotective effects against rotenone-induced Parkinson in mice regarding both motor dysfunction and neurodegeneration. Betanin’s neurohealth benefit relates to its powerful antioxidative property. Therefore, betanin use in neurodegenerative disease therapy is interesting to study.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
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