Ecklonia cava polyphenols (ECPs) show promise in reducing neuronal damage caused by rotenone in Parkinson’s disease (PD) by activating the Nrf2-ARE pathway, highlighting their potential as a neuroprotective treatment.
By Dr. Priyom Bose, Ph.D.Reviewed by Benedette Cuffari, M.Sc.Aug 7 2024 A recent Nutrients study evaluates the neuroprotective properties of Ecklonia cava polyphenols in alleviating neuronal damage caused by rotenone in Parkinson’s disease .
Due to the rapid aging of the global population, PD cases are estimated to reach 14.2 million by 2040. To date, scientists have failed to develop any treatment to attenuate the progression of PD. Rotenone, derived from the roots of tropical legumes like couve, is commonly used as an insecticide and pesticide. Previous studies have shown that oral rotenone administration causes motor and gastrointestinal dysfunction. Mechanistically, rotenone triggers mitochondrial dysfunction by inhibiting respiratory chain electron transport complex I, which subsequently increases ROS generation and apoptosis.
Therefore, the Nrf2-ARE pathway could be targeted to protect neurons from oxidative stress using antioxidants. This concept could be exploited in PD prevention and treatment. After acclimatizing mice to laboratory conditions, they were randomly assigned to the control, rotenone, ECP, and ECP groups, each comprising six mice. In the ECP group, mice were treated with 20 mg/kg ECP, whereas mice in the ECP group were treated with 240 mg/kg ECP. All mice were orally administered rotenone daily for 30 days except for the control group.
Nrf2 mediates induction of the p62 gene, which supports Nrf2 activation through a positive feedback loop. Following ECP treatment of rotenone-exposed cells, a significant increase in p62 messenger ribonucleic acid levels was observed.
Anti-Inflammatory Antioxidant Autosomal Cell Colon Depression Dopaminergic In Vitro Intracellular Neurodegenerative Disorder Neurons Nutrients Oxidative Stress Oxygen Polyphenol Protein Stress Tremor
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