Summary:
Parkinson’s disease (PD) is one of the most common neurodegenerative disorders globally. Its risk increases significantly with age, tripling every decade after the age of 60. PD presents with motor symptoms such as tremor and slowness of movement, as well as non-motor symptoms like depression and cognitive impairment. Although therapeutic management can alleviate some symptoms, PD remains a progressive condition with no known cure. This study focused on sporadic PD, a subset of the disease. The primary risk factors include genetic predispositions and environmental exposures, particularly to neurotoxic substances such as pesticides, which are harmful to the human nervous system. While the precise mechanisms are not entirely understood, factors such as oxidative stress induced by these chemicals, mitochondrial dysfunction, abnormal accumulation of problematic proteins, and inflammation are all implicated in PD pathogenesis. Rotenone, a pesticide derived from the roots of tropical legumes, is known to induce mitochondrial dysfunction. Oral administration of rotenone has been associated with motor and gastrointestinal dysfunctions, as well as a reduction in neuron function. For this reason, rotenone was used in this study to create PD models in laboratory settings, both in vitro and in vivo in mice. This study aimed to investigate the neuroprotective effects of Ecklonia cava polyphenols (ECP), a polyphenol unique to brown algae, against rotenone-induced damage to neurons. The study focused on its antioxidant properties. Using human cells and PD model mice, the researchers found that ECP enhanced the expression and activity of antioxidant enzymes. In PD model mice, ECPs improved motor function impaired by rotenone and restored both intestinal motor function and colon tissue. Additionally, ECPs had a protective effect on dopaminergic neurons. These findings indicate that ECP may have a preventative effect on PD.
Abstract:
Parkinson’s disease (PD) is a degenerative neurological disorder defined by the deterioration and loss of dopamine-producing neurons in the substantia nigra, leading to a range of motor impairments and non-motor symptoms. The underlying mechanism of this neurodegeneration remains unclear. This research examined the neuroprotective properties of Ecklonia cava polyphenols (ECPs) in mitigating neuronal damage induced by rotenone via the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)–antioxidant response element (ARE) pathway. Using human neuroblastoma SH-SY5Y cells and PD model mice, we found that ECP, rich in the antioxidant polyphenol phlorotannin, boosted the gene expression and functionality of the antioxidant enzyme NAD(P)H quinone oxidoreductase-1. ECP also promoted Nrf2 nuclear translocation and increased p62 expression, suggesting that p62 helps sustain Nrf2 activation via a positive feedback loop. The neuroprotective effect of ECP was significantly reduced by Compound C (CC), an AMP-activated protein kinase (AMPK) inhibitor, which also suppressed Nrf2 nuclear translocation.
Article Publication Date: 30/05/2024
DOI: 10.3390/nu16132076
