Asiatic Acid Prevents Oxidative Stress and Apoptosis by Inhibiting the Translocation of α-Synuclein Into Mitochondria

Ding, Hongqun; Xiong, Yuyun; Sun, Jing; Chen, Chen; Gao, Jing; Xu, Huaxi

doi:10.3389/fnins.2018.00431

Cited by 33 publications

(26 citation statements)

References 41 publications

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“…Application of oligomeric α-synuclein increases ROS production and lipid peroxidation [ 24 , 25 ]. α-synuclein is translocated to mitochondria and directly interacts with mitochondrial proteins including ATP synthase to lower mitochondrial inner membrane potential, thus altering neuronal energy metabolism and opening mitochondrial death channels [ 24 , 26 ]. Increased oxidative stress induced by treatment with hydrogen peroxide or depletion of antioxidant enzymes enhances post-translational modification and aggregation of α-synuclein and worsens the progression of PD [ 27 , 28 , 29 ].…”

Section: Oxidative Stress and Park Genesmentioning

confidence: 99%

Dietary Antioxidants and Parkinson’s Disease

Park

Ellis

2020

Antioxidants

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Parkinson’s disease (PD) is a neurodegenerative disorder caused by the depletion of dopaminergic neurons in the basal ganglia, the movement center of the brain. Approximately 60,000 people are diagnosed with PD in the United States each year. Although the direct cause of PD can vary, accumulation of oxidative stress-induced neuronal damage due to increased production of reactive oxygen species (ROS) or impaired intracellular antioxidant defenses invariably occurs at the cellular levels. Pharmaceuticals such as dopaminergic prodrugs and agonists can alleviate some of the symptoms of PD. Currently, however, there is no treatment to halt the progression of PD pathology. Due to the nature of PD, a long and progressive neurodegenerative process, strategies to prevent or delay PD pathology may be well suited to lifestyle changes like dietary modification with antioxidant-rich foods to improve intracellular redox homeostasis. In this review, we discuss cellular and genetic factors that increase oxidative stress in PD. We also discuss neuroprotective roles of dietary antioxidants including vitamin C, vitamin E, carotenoids, selenium, and polyphenols along with their potential mechanisms to alleviate PD pathology.

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Section: Oxidative Stress and Park Genesmentioning

confidence: 99%

Dietary Antioxidants and Parkinson’s Disease

Park

Ellis

2020

Antioxidants

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“…In relation to mitochondria, the triterpenoid, asiatic acid, reportedly protects neurons from cell death by preventing mitochondria-dependent apoptosis in a cellular model of AD [297]. Another study also demonstrated that asiatic acid blocked the translocation of α -synuclein into mitochondria, thereby protecting it against oxidative stress and apoptosis [298]. Asiatic acid also prevented the α -synuclein-induced decrease in mitochondrial membrane potential in a Drosophila model of PD [298].…”

Section: Mitochondrial Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

“…Another study also demonstrated that asiatic acid blocked the translocation of α -synuclein into mitochondria, thereby protecting it against oxidative stress and apoptosis [298]. Asiatic acid also prevented the α -synuclein-induced decrease in mitochondrial membrane potential in a Drosophila model of PD [298].…”

Section: Mitochondrial Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis

Huang

Chiang

Kalinowski

et al. 2019

Oxidative Medicine and Cellular Longevity

104

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The mitochondrion is an essential organelle important for the generation of ATP for cellular function. This is especially critical for cells with high energy demands, such as neurons for signal transmission and cardiomyocytes for the continuous mechanical work of the heart. However, deleterious reactive oxygen species are generated as a result of mitochondrial electron transport, requiring a rigorous activation of antioxidative defense in order to maintain homeostatic mitochondrial function. Indeed, recent studies have demonstrated that the dysregulation of antioxidant response leads to mitochondrial dysfunction in human degenerative diseases affecting the nervous system and the heart. In this review, we outline and discuss the mitochondrial and oxidative stress factors causing degenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Friedreich’s ataxia. In particular, the pathological involvement of mitochondrial dysfunction in relation to oxidative stress, energy metabolism, mitochondrial dynamics, and cell death will be explored. Understanding the pathology and the development of these diseases has highlighted novel regulators in the homeostatic maintenance of mitochondria. Importantly, this offers potential therapeutic targets in the development of future treatments for these degenerative diseases.

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“…Finally, the cells were photographed with a fluorescence microscope (Nikon, Japan) at Ex488 nm/Em535 nm and Ex 540 mm/Em570 nm[34].2.11. In Vivo Mouse Model Experiments.…”

mentioning

confidence: 99%

Baicalin Represses C/EBPβ via Its Antioxidative Effect in Parkinson’s Disease

Lei

Shen

et al. 2020

Oxidative Medicine and Cellular Longevity

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Parkinson’s disease (PD) is a neurodegenerative disease characterized by the gradual loss of dopaminergic (DA) neurons in the substantia nigra (SN) and the formation of intracellular Lewy bodies (LB) in the brain, which aggregates α-synuclein (α-Syn) as the main component. The interest of flavonoids as potential neuroprotective agents is increasing due to its high efficiency and low side effects. Baicalin is one of the flavonoid compounds, which is a predominant flavonoid isolated from Scutellaria baicalensis Georgi. However, the key molecular mechanism by which Baicalin can prevent the PD pathogenesis remains unclear. In this study, we used bioinformatic assessment including Gene Ontology (GO) to elucidate the correlation between oxidative stress and PD pathogenesis. RNA-Seq methods were used to examine the global expression profiles of noncoding RNAs and found that C/EBPβ expression was upregulated in PD patients compared with healthy controls. Interestingly, Baicalin could protect DA neurons against reactive oxygen species (ROS) and decreased C/EBPβ and α-synuclein expression in pLVX-Tet3G-α-synuclein SH-SY5Y cells. In a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced PD mouse model, the results revealed that treatment with Baicalin improved the PD model’s behavioral performance and reduced dopaminergic neuron loss in the substantia nigra, associated with the inactivation of proinflammatory cytokines and oxidative stress. Hence, our study supported that Baicalin repressed C/EBPβ via redox homeostasis, which may be an effective potential treatment for PD.

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Asiatic Acid Prevents Oxidative Stress and Apoptosis by Inhibiting the Translocation of α-Synuclein Into Mitochondria

Cited by 33 publications

References 41 publications

Dietary Antioxidants and Parkinson’s Disease

Dietary Antioxidants and Parkinson’s Disease

The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis

Baicalin Represses C/EBPβ via Its Antioxidative Effect in Parkinson’s Disease

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