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Research Article | Volume 13 Issue 11 (Nov, 2023) | Pages 224 - 230
Evaluation of Neuroprotective Effects of Metformin in Rotenone- Induced Parkinson's Disease in Drosophila Melanogaster
Under a Creative Commons license
Open Access
Received
Oct. 2, 2023
Revised
Oct. 16, 2023
Accepted
Nov. 3, 2023
Published
Nov. 24, 2023
Abstract

Introduction: Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease, mainly affecting elderly people. It is caused by degeneration of dopaminergic neurons in the striatum. Metformin, by activating AMP-activated protein kinase (AMPK), induces autophagy and reduces reactive oxygen species (ROS) production, leading to a reduction in neuroinflammation. Thus, the study was designed to assess the neuroprotective effect of Metformin in the rotenone-induced Parkinson's model of Drosophila melanogaster. Materials and Method: Drosophila flies were cultured in cornmeal agar medium. Seven-day-old flies were divided into five groups with approximately 30 flies in each group: normal control, disease control, Levodopa (1 mM), and Metformin low dose (20 mM) and high dose (40 mM). Rotenone (125 μM) was used to induce the disease. All drugs were administered through the cornmeal agar medium for seven days, and on the eighth day, a climbing assay was performed. Effect on biochemical variables like Malondialdehyde (MDA) and Dopamine levels in the Drosophila brain were also assessed. Result: There was a significant improvement in the flying and climbing ability of Drosophila flies in the metformin (high and low doses) and L-dopa groups compared to the disease control group. Also, there was a significant increase in levels of Dopamine and a decrease in levels of MDA in the Drosophila brain in the metformin-treated groups and the L-dopa group. All these effects were most pronounced in the group receiving a high dose of metformin. Conclusion: Metformin was found to be neuroprotective as it improved the locomotor activity of Drosophila flies, probably by reducing oxidative stress and degeneration of dopaminergic neurons.

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