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Oral Administration of Rotenone using a Gavage and Image Analysis of Alpha-synuclein Inclusions in the Enteric Nervous System
Published on: October 26, 2010
Benefits of betanin in rotenone-induced Parkinson mice
Wachiryah Thong-Asa1, Sujira Jedsadavitayakol2, Suchawalee Jutarattananon2
1Animal Toxicology and Physiology Specialty Research Unit (ATPSRU), Physiology Division, Department of Zoology, Faculty of Science, Kasetsart University, 50 Ngamwongwan road, Jatuchak, Bangkok, 10900, Thailand. fsciwyth@ku.ac.th.
Abstract:
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 at 2.5 mg/kg/48 h was subcutaneous injected in Rot groups, and betanin at 100 and 200 mg/kg/48 h were given alternately with the rotenone injections in Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Brain oxidative status including malondialdehyde, reduced glutathione, catalase, superoxide dismutase, with neuronal degeneration in the motor cortex, striatum and substantia nigra par compacta were evaluated. The immunohistochemical densities of tyrosine hydroxylase in striatum and in substantia nigra par compacta 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 substantia nigra par compacta, striatum and motor cortex significantly increased (p < 0.05), and the tyrosine hydroxylase density in substantia nigra par compacta and in striatum significantly decreased (p < 0.05). Betanin at 100 and 200 mg/kg significantly prevented substantia nigra par compacta, striatum and motor cortex neuronal degeneration (p < 0.05) and maintained tyrosine hydroxylase density in substantia nigra par compacta and in striatum (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 malondialdehyde levels and boosted reduced glutathione, catalase and superoxide dismutase 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 is interesting to study.
Insights
Betanin demonstrated significant neuroprotective effects in a mouse model of Parkinson disease. This natural compound reduced motor deficits and neurodegeneration by combating oxidative stress.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Parkinson disease is a neurodegenerative disorder characterized by motor dysfunction and neuronal loss.
- Rotenone is a pesticide that induces Parkinson-like symptoms in animal models.
- Oxidative stress plays a crucial role in the pathogenesis of Parkinson disease.
Purpose of the Study:
- To investigate the neuroprotective potential of betanin against rotenone-induced Parkinsonism in mice.
- To evaluate the effects of betanin on motor function, neurodegeneration, and oxidative stress markers.
Main Methods:
- Male ICR mice were administered rotenone to induce Parkinson-like symptoms.
- Mice were treated with varying doses of betanin (100 and 200 mg/kg).
- Motor function was assessed using hanging wire and rotarod tests.
- Brain tissue analysis included evaluation of oxidative stress markers and neuronal degeneration, along with tyrosine hydroxylase density.
Main Results:
- Rotenone administration significantly impaired motor function and caused neuronal degeneration in the motor cortex, striatum, and substantia nigra.
- Betanin treatment dose-dependently ameliorated motor deficits and reduced neuronal degeneration.
- Betanin treatment significantly attenuated oxidative stress by reducing malondialdehyde and increasing glutathione, catalase, and superoxide dismutase levels.
- Tyrosine hydroxylase density in the striatum and substantia nigra was preserved in betanin-treated groups.
Conclusions:
- Betanin exhibits significant neuroprotective effects against rotenone-induced Parkinsonism in mice.
- The neuroprotective benefits of betanin are attributed to its potent antioxidant properties.
- Betanin holds promise as a therapeutic agent for neurodegenerative diseases like Parkinson disease.
