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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
Morin ameliorates rotenone-induced Parkinson disease in mice through antioxidation and anti-neuroinflammation:
I O Ishola1, I O Awogbindin2, T G Olubodun-Obadun1
1Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Lagos State, Nigeria.
Abstract:
Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting both motor and non-motor functions. It is well reported that the neuropathological process leading to PD starts from the gut before spreading to the CNS affirming the role of environmental toxicants such as rotenone. Morin (3, 5, 7, 2', 4'-pentahydroxyflavone) possesses neuroprotective and anti-oxidant activities which could be beneficial in PD. This study was designed to investigate the ameliorative influence of morin on rotenone-induced PD in mice. Male albino mice (18-23 g) were randomly divided into groups (n = 15) and treated for 28 consecutive days as follows: group 1: normal saline (10 ml/kg, p.o); group 2: rotenone (1 mg/kg, p.o, 0.5%w/v in CMC); groups 3-5: morin (5, 20 or 80 mg/kg, i.p.) + rotenone (1 mg/kg, p.o.), respectively, group 6: morin (20 mg/kg only, i.p.). Behavioural tasks were carried out weekly 1 h after treatments. Mice were euthanized on day 28 and discreet brain regions were assayed for oxidative stress parameters and immunohistochemical analysis. Morin reversed rotenone-induced behavioural deficits (motor incoordination, working memory deficit and depressive-like behaviour). Moreso, rotenone-induced lipid peroxidation (MDA), with a concomitant decrease in glutathione (GSH), superoxide dismutase (SOD) and acetylcholinesterase (AchE) activities in discreet regions of the brain were attenuated by the pre-treatment of mice with morin. Rotenone caused significant increase in the expression of iba-1, glial fibrillary acidic protein (GFAP), toll-like receptor 4 (TLR-4), and α-synuclein with a decrease in tyrosine hydroxylase positive neurons (TH) expression which were ameliorated by the pretreatment of mice with morin. Furthermore, rotenone-induced colon necrosis was reversed by morin administration. This study lend credence to the neuroprotective action of morin on rotenone-induced PD through enhancement of antioxidant defense and anti-inflammatory mechanisms.
Insights
Morin, a natural compound, demonstrated significant neuroprotective effects against rotenone-induced Parkinson's disease (PD) in mice. It improved motor function, memory, and reduced inflammation, offering a potential therapeutic strategy for PD.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Parkinson's disease (PD) is a progressive neurodegenerative disorder impacting motor and non-motor functions, with environmental toxicants like rotenone implicated in its pathology.
- The gut-brain axis plays a role in PD pathogenesis, suggesting environmental factors can initiate neurodegenerative processes.
- Morin, a flavonoid, exhibits known antioxidant and neuroprotective properties, making it a candidate for investigating PD interventions.
Purpose of the Study:
- To investigate the potential therapeutic effects of morin on rotenone-induced Parkinson's disease (PD) in a mouse model.
- To evaluate morin's impact on behavioral deficits, oxidative stress, neuroinflammation, and alpha-synuclein aggregation in the context of PD.
Main Methods:
- Male albino mice were administered rotenone to induce PD-like symptoms and treated with varying doses of morin or saline for 28 days.
- Behavioral tests assessed motor coordination, memory, and depressive-like behaviors weekly.
- Brain and colon tissues were analyzed for oxidative stress markers, neuroinflammation (Iba-1, GFAP, TLR-4), alpha-synuclein, tyrosine hydroxylase (TH) positive neurons, and colon necrosis.
Main Results:
- Morin administration significantly reversed rotenone-induced motor deficits, memory impairment, and depressive-like behaviors.
- Morin treatment attenuated rotenone-induced lipid peroxidation and restored levels of glutathione and superoxide dismutase in the brain.
- Morin reduced the expression of inflammatory markers (Iba-1, GFAP, TLR-4) and alpha-synuclein, while increasing TH-positive neurons, and also reversed rotenone-induced colon necrosis.
Conclusions:
- Morin exhibits significant neuroprotective effects against rotenone-induced Parkinson's disease in mice.
- The protective mechanisms of morin involve enhancing antioxidant defense, reducing neuroinflammation, and mitigating alpha-synuclein pathology.
- Morin demonstrates potential as a therapeutic agent for Parkinson's disease, addressing both central nervous system and gut-related pathology.
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