Phloretin attenuates behavior deficits and neuroinflammatory response in MPTP induced Parkinson's disease in mice

Zhang, Gejuan; Yang, Guanghui; Liu, Jian

doi:10.1016/j.lfs.2019.116600

Cited by 26 publications

(16 citation statements)

References 43 publications

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“…Minor flavonoids: Genistein, an isoflavone abundantly found in soy bean, has been revealed to exert a protective mechanism through the restoration of decreased mitochondrial membrane potential in 6-OHDA-treated SK-N-SH neuroblastoma cells ( Table 3 ) [ 180 , 190 ]. Phloretin (chalcones) can protect DA neuron and attenuate behavior deficits through inhibition of oxidative stress and neuroinflammation in an MPTP-induced mouse model of PD ( Table 3 ) [ 191 , 192 ].…”

Section: Natural Antioxidants: Flavonoidsmentioning

confidence: 99%

“…The anti-inflammatory effect is well identified as a health-promoting property of flavonoids following the anti-oxidative effect. Several studies of in vivo and in vitro identified that flavonoids, such as naringin [ 136 , 138 ], silibinin [ 146 , 153 ], myricitrin [ 197 ], nobiletin [ 198 ], and astilbin [ 164 ], protect the DA neurons and/or DA axons against neurotoxin-induced neurodegeneration by suppressing the microglial activation and the subsequent release of pro-inflammatory cytokines, such as TNF-α and IL-1β [ 148 , 150 , 192 , 193 ]. Moreover, silibinin preserves the locomotor activity in the prothrombin kringle-2 (an endogenous microglial activator)-treated models, through the downregulation of ERK1/2 signaling pathway [ 146 ].…”

Section: Natural Antioxidants: Flavonoidsmentioning

confidence: 99%

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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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Section: Natural Antioxidants: Flavonoidsmentioning

confidence: 99%

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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“…MPTP-induced reduced dopamine (DA) levels, motor abnormalities, reduced tyrosine hydroxylase (TH) enzyme protein expression and inflammation were significantly improved by phloretin. Improvements in levels of specific inflammatory markers like glial fibrillary acidic protein (GFAP), proinflammatory cytokines such as IL-β, IL-6, and TNF-α have been proposed to play an important role in the neuroprotective effect of phloretin and treatment has been reported to be promising for Parkinson's disease [25].…”

Section: Current Treatment Approaches Associated With Cytokinesmentioning

confidence: 99%

Proinflammatory cytokines in Parkinson’s disease and current treatment approaches

Ahmet¹

2020

GSC Adv. Res. Rev.

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Parkinson's disease is a neurodegenerative disease characterized by progressive degeneration of dopaminergic neurons in the substantia nigra region. As the etiology is not clear, treatment in this disease is rather symptomatic and inadequate to prevent the progression of the disease. However, recent studies have demonstrated the strong association of neuroinflammation and proinflammatory cytokines with disease pathology. In this review, the relationship of proinflammatory cytokines with the pathology of Parkinson's disease is discussed and current treatment approaches targeting these mechanisms are evaluated.

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“…A special mention must be done for exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridine (MPTP), with similar structure of some herbicides that increase the risk of PD, due to its historical importance. Since its incidental discovery in drug abusers after inadvertent self-administration, MPTP has been widely used to induce PD in animal models (Zhang et al, 2019). MPTP is lipid-soluble molecule that penetrates the blood–brain barrier and, once converted to its oxidized product (MPP+), interferes with mitochondrial respiration.…”

Section: Parkinson’s Diseasementioning

confidence: 99%

Bioenergetics and Autophagic Imbalance in Patients-Derived Cell Models of Parkinson Disease Supports Systemic Dysfunction in Neurodegeneration

et al. 2019

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Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder worldwide affecting 2–3% of the population over 65 years. This prevalence is expected to rise as life expectancy increases and diagnostic and therapeutic protocols improve. PD encompasses a multitude of clinical, genetic, and molecular forms of the disease. Even though the mechanistic of the events leading to neurodegeneration remain largely unknown, some molecular hallmarks have been repeatedly reported in most patients and models of the disease. Neuroinflammation, protein misfolding, disrupted endoplasmic reticulum-mitochondria crosstalk, mitochondrial dysfunction and consequent bioenergetic failure, oxidative stress and autophagy deregulation, are amongst the most commonly described. Supporting these findings, numerous familial forms of PD are caused by mutations in genes that are crucial for mitochondrial and autophagy proper functioning. For instance, late and early onset PD associated to mutations in Leucine-rich repeat kinase 2 (LRRK2) and Parkin (PRKN) genes, responsible for the most frequent dominant and recessive inherited forms of PD, respectively, have emerged as promising examples of disease due to their established role in commanding bioenergetic and autophagic balance. Concomitantly, the development of animal and cell models to investigate the etiology of the disease, potential biomarkers and therapeutic approaches are being explored. One of the emerging approaches in this context is the use of patient’s derived cells models, such as skin-derived fibroblasts that preserve the genetic background and some environmental cues of the patients. An increasing number of reports in these PD cell models postulate that deficient mitochondrial function and impaired autophagic flux may be determinant in PD accelerated nigral cell death in terms of limitation of cell energy supply and accumulation of obsolete and/or unfolded proteins or dysfunctional organelles. The reliance of neurons on mitochondrial oxidative metabolism and their post-mitotic nature, may explain their increased vulnerability to undergo degeneration upon mitochondrial challenges or autophagic insults. In this scenario, proper mitochondrial function and turnover through mitophagy, are gaining in strength as protective targets to prevent neurodegeneration, together with the use of patient-derived fibroblasts to further explore these events. These findings point out the presence of molecular damage beyond the central nervous system (CNS) and proffer patient-derived cell platforms to the clinical and scientific community, which enable the study of disease etiopathogenesis and therapeutic approaches focused on modifying the natural history of PD through, among others, the enhancement of mitochondrial function and autophagy.

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Phloretin attenuates behavior deficits and neuroinflammatory response in MPTP induced Parkinson's disease in mice

Cited by 26 publications

References 43 publications

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

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

Proinflammatory cytokines in Parkinson’s disease and current treatment approaches

Bioenergetics and Autophagic Imbalance in Patients-Derived Cell Models of Parkinson Disease Supports Systemic Dysfunction in Neurodegeneration

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