Cyanidin Protects SH-SY5Y Human Neuroblastoma Cells from 1-Methyl-4-Phenylpyridinium-Induced Neurotoxicity

Chen, Jian; Sun, Jian; Jiang, Julian; Zhou, Jie

doi:10.1159/000489853

Cited by 15 publications

(6 citation statements)

References 26 publications

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“…Similar results were observed in SH-SY5Y cells treated with the aglycon, cyanidin, and 1-methyl-4-phenylpyridinium (MPP + ), which acts as a mitochondrial complex I inhibitor to induce neurotoxicity [120,121]. In this model, cyanidin treatment dose-dependently prevented cell death, and lowered the ratio of Bax:Bcl-2 ratio [120]. This has been further validated in vivo in a study demonstrating that anthocyanin treatment significantly reduced both the Bad:Bcl-xL ratio and the Bax:Bcl-2 ratio, and increased cellular survival in a rat model of ischemic stroke [91].…”

Section: The Use Of Anthocyanins As Novel Neuroprotective and Thersupporting

confidence: 54%

“…Indeed, in a cellular model of 6-hydroxydopamine (6-OHDA) toxicity, a chemical often used to induce a Parkinsonian phenotype in mice and rats, treatment with an anthocyanin-rich extract from mulberry elevated expression of pro-survival Bcl-2 protein while suppressing expression of the pro-apoptotic Bax protein [119]. Similar results were observed in SH-SY5Y cells treated with the aglycon, cyanidin, and 1-methyl-4-phenylpyridinium (MPP + ), which acts as a mitochondrial complex I inhibitor to induce neurotoxicity [120,121]. In this model, cyanidin treatment dose-dependently prevented cell death, and lowered the ratio of Bax:Bcl-2 ratio [120].…”

Section: The Use Of Anthocyanins As Novel Neuroprotective and Thermentioning

confidence: 87%

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Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

2019

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Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS), are characterized by the death of neurons within specific regions of the brain or spinal cord. While the etiology of many neurodegenerative diseases remains elusive, several factors are thought to contribute to the neurodegenerative process, such as oxidative and nitrosative stress, excitotoxicity, endoplasmic reticulum stress, protein aggregation, and neuroinflammation. These processes culminate in the death of vulnerable neuronal populations, which manifests symptomatically as cognitive and/or motor impairments. Until recently, most treatments for these disorders have targeted single aspects of disease pathology; however, this strategy has proved largely ineffective, and focus has now turned towards therapeutics which target multiple aspects underlying neurodegeneration. Anthocyanins are unique flavonoid compounds that have been shown to modulate several of the factors contributing to neuronal death, and interest in their use as therapeutics for neurodegeneration has grown in recent years. Additionally, due to observations that the bioavailability of anthocyanins is low relative to that of their metabolites, it has been proposed that anthocyanin metabolites may play a significant part in mediating the beneficial effects of an anthocyanin-rich diet. Thus, in this review, we will explore the evidence evaluating the neuroprotective and therapeutic potential of anthocyanins and their common metabolites for treating neurodegenerative diseases.

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Section: The Use Of Anthocyanins As Novel Neuroprotective and Thersupporting

confidence: 54%

Section: The Use Of Anthocyanins As Novel Neuroprotective and Thermentioning

confidence: 87%

Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

2019

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“…Pelargonidin alleviates 6-OHDA-induced neurotoxicity through the suppression of lipid oxidation in a rodent model of PD. Blueberry extracts, such as pelargonidin, peonidin, and petunidin, have multiple health-promoting properties, and it has been largely revealed that blueberries and pomegranate extract can protect neurons against neurotoxic events, such as apoptosis, inflammation, and OS ( Table 3 ) [ 187 , 188 , 189 ].…”

Section: Natural Antioxidants: Flavonoidsmentioning

confidence: 99%

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

et al. 2020

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Oxidative stress reflects an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems, and it can be associated with the pathogenesis and progression of neurodegenerative diseases such as multiple sclerosis, stroke, and Parkinson’s disease (PD). The application of antioxidants, which can defend against oxidative stress, is able to detoxify the reactive intermediates and prevent neurodegeneration resulting from excessive ROS production. There are many reports showing that numerous flavonoids, a large group of natural phenolic compounds, can act as antioxidants and the application of flavonoids has beneficial effects in the adult brain. For instance, it is well known that the long-term consumption of the green tea-derived flavonoids catechin and epigallocatechin gallate (EGCG) can attenuate the onset of PD. Also, flavonoids such as ampelopsin and pinocembrin can inhibit mitochondrial dysfunction and neuronal death through the regulation of gene expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Additionally, it is well established that many flavonoids exhibit anti-apoptosis and anti-inflammatory effects through cellular signaling pathways, such as those involving (ERK), glycogen synthase kinase-3β (GSK-3β), and (Akt), resulting in neuroprotection. In this review article, we have described the oxidative stress involved in PD and explained the therapeutic potential of flavonoids to protect the nigrostriatal DA system, which may be useful to prevent PD.

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“…1-Methyl-4-phenylpyridinium (ion) (MPP+) is a dopamine neurotoxin, which can induce parkinsonism [55]. MPP+ is widely used in the study of Parkinson's disease in various animal cell models [56,57]. In SH-SY5Y cells, the expression of sestrin2, p53, and levels of ROS were induced by MPP+, while the increased expression of sestrin2 induced by MPP+ was abolished by the downregulation of p53 at both the mRNA and protein levels.…”

Section: Antioxidant Activity Of P53 In Chemically Induced Oxidative mentioning

confidence: 99%

Functional Role of p53 in the Regulation of Chemical-Induced Oxidative Stress

Liu

Fan

et al. 2020

Oxidative Medicine and Cellular Longevity

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The nuclear transcription factor p53, discovered in 1979, has a broad range of biological functions, primarily the regulation of apoptosis, the cell cycle, and DNA repair. In addition to these canonical functions, a growing body of evidence suggests that p53 plays an important role in regulating intracellular redox homeostasis through transcriptional and nontranscriptional mechanisms. Oxidative stress induction and p53 activation are common responses to chemical exposure and are suggested to play critical roles in chemical-induced toxicity. The activation of p53 can exert either prooxidant or antioxidant activity, depending on the context. In this review, we discuss the functional role of p53 in regulating chemical-induced oxidative stress, summarize the potential signaling pathways involved in p53’s regulation of chemically mediated oxidative stress, and propose issues that should be addressed in future studies to improve understanding of the relationship between p53 and chemical-induced oxidative stress.

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Cyanidin Protects SH-SY5Y Human Neuroblastoma Cells from 1-Methyl-4-Phenylpyridinium-Induced Neurotoxicity

Cited by 15 publications

References 26 publications

Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

Functional Role of p53 in the Regulation of Chemical-Induced Oxidative Stress

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