Lutein protects dopaminergic neurons against MPTP-induced apoptotic death and motor dysfunction by ameliorating mitochondrial disruption and oxidative stress
| Autor: | Thamilarasan Manivasagam, Jagatheesan Nataraj, Arokiyasamy Justin Thenmozhi, Musthafa Mohammed Essa |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Male Lutein Parkinson's disease Antioxidant medicine.medical_treatment Dopamine Medicine (miscellaneous) Apoptosis Nerve Tissue Proteins Oxidative phosphorylation Pharmacology Biology Motor Activity medicine.disease_cause Antiparkinson Agents 03 medical and health sciences chemistry.chemical_compound Random Allocation 0302 clinical medicine medicine Neurotoxin Animals Nutrition and Dietetics Behavior Animal General Neuroscience MPTP Dopaminergic Neurons food and beverages MPTP Poisoning Parkinson Disease General Medicine medicine.disease eye diseases Mitochondria Mice Inbred C57BL Substantia Nigra Oxidative Stress 030104 developmental biology Neuroprotective Agents Biochemistry chemistry Dietary Supplements Apoptosis Regulatory Proteins 030217 neurology & neurosurgery Oxidative stress Biomarkers |
| Zdroj: | Nutritional neuroscience. 19(6) |
| ISSN: | 1476-8305 |
| Popis: | Mitochondrial dysfunction and oxidative stress-mediated apoptosis plays an important role in various neurodegenerative diseases including Huntington's disease, Parkinson's disease (PD) and Alzheimer's disease (AD). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the most widely used neurotoxin mimics the symptoms of PD by inhibiting mitochondrial complex I that stimulates excessive intracellular reactive oxygen species (ROS) and finally leads to mitochondrial-dependent apoptosis. Lutein, a carotenoid of xanthophyll family, is found abundantly in leafy green vegetables such as spinach, kale and in egg yolk, animal fat and human eye retinal macula. Increasing evidence indicates that lutein has offers benefits against neuronal damages during diabetic retinopathy, ischemia and AD by virtue of its mitochondrial protective, antioxidant and anti-apoptotic properties.Male C57BL/6 mice (23-26 g) were randomized and grouped in to Control, MPTP, and Lutein treated groups.Lutein significantly reversed the loss of nigral dopaminergic neurons by increasing the striatal dopamine level in mice. Moreover, lutein-ameliorated MPTP induced mitochondrial dysfunction, oxidative stress and motor abnormalities. In addition, lutein repressed the MPTP-induced neuronal damage/apoptosis by inhibiting the activation of pro-apoptotic markers (Bax, caspases-3, 8 and 9) and enhancing anti-apoptotic marker (Bcl-2) expressions.Our current results revealed that lutein possessed protection on dopaminergic neurons by enhancing antioxidant defense and diminishing mitochondrial dysfunction and apoptotic death, suggesting the potential benefits of lutein for PD treatment. |
| Databáze: | OpenAIRE |
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