Epicatechin Reduces Striatal MPP<sup>+</sup>-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity

Rubio-Osornio, Moisés; Gorostieta-Salas, Elisa; Montes, Sergio; Pérez-Severiano, Francisca; Rubio, Carmen; Gómez, Clarisa Villegas; Rı́os, Camilo; Guevara, Jorge

doi:10.1155/2015/276039

Cited by 12 publications

(10 citation statements)

References 26 publications

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“…Many studies have demonstrated that MPTP or MPP + causes oxidative stress, including carbonyl and other forms of protein oxidation. 40-43 Oxidative stress correlates with a shift of pI of PARK7 to be more acidic. 33 Our recent studies have shown that oxidative stress-induced carbonyl oxidation of MEF2D correlates with its migration to the acidic range.…”

Section: Discussionmentioning

confidence: 99%

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

et al. 2016

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As a selective degradation system, chaperone-mediated autophagy (CMA) is essential for maintaining cellular homeostasis and survival under stress conditions. Increasing evidence points to an important role for the dysfunction of CMA in the pathogenesis of Parkinson disease (PD). However, the mechanisms by which CMA regulates neuronal survival under stress and its role in neurodegenerative diseases are not fully understood. PARK7/DJ-1 is an autosomal recessive familial PD gene. PARK7 plays a critical role in antioxidative response and its dysfunction leads to mitochondrial defects. In the current study, we showed that CMA mediated the lysosome-dependent degradation of PARK7. Importantly, CMA preferentially removed the oxidatively damaged nonfunctional PARK7 protein. Furthermore, CMA protected cells from mitochondrial toxin MPP+-induced changes in mitochondrial morphology and function, and increased cell viability. These protective effects were lost under PARK7-deficiency conditions. Conversely, overexpression of PARK7 significantly attenuated the mitochondrial dysfunction and cell death exacerbated by blocking CMA under oxidative stress. Thus, our findings reveal a mechanism by which CMA protects mitochondrial function by degrading nonfunctional PARK7 and maintaining its homeostasis, and dysregulation of this pathway may contribute to the neuronal stress and death in PD pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

et al. 2016

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“…Rubio-Osornio et al (2015) administered 10 µg of MPP + (in 8 µL saline) intrastriatal into the right striatum to induce the neurotoxicity in male Wistar rats and assessed the epicatechin activity (40, 60, and 80 mg/kg, oral administration for five days). They applied an apomorphine-induced (1 mg/kg, subcutaneously for six days after MPP + -injection) circling behavior test and revealed that MPP + -induction increased the turning behaviors, where the subchronic dose of epicatechin at 100 mg/kg decreased the turning behavior in MPP + -induced rats [ 164 ]. Aguirre-Vidal et al (2017) administered 15 µg of MPP + (in 8 µL saline) intrastriatal on the 6th day, into the right striatum in male Wistar rats and evaluated the effect of β-estradiol-3-benzoate (100 µg/kg, for every 48 h for 11 days) against MPP + toxicity.…”

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Prasad

Hung

2020

Antioxidants

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Currently, neurodegenerative diseases are a major cause of disability around the world. Parkinson’s disease (PD) is the second-leading cause of neurodegenerative disorder after Alzheimer’s disease. In PD, continuous loss of dopaminergic neurons in the substantia nigra causes dopamine depletion in the striatum, promotes the primary motor symptoms of resting tremor, bradykinesia, muscle rigidity, and postural instability. The risk factors of PD comprise environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular injury, aging, and hereditary defects. The pathologic features of PD include impaired protein homeostasis, mitochondrial dysfunction, nitric oxide, and neuroinflammation, but the interaction of these factors contributing to PD is not fully understood. In neurotoxin-induced PD models, neurotoxins, for instance, 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-Methyl-4-phenylpyridinium (MPP+), paraquat, rotenone, and permethrin mainly impair the mitochondrial respiratory chain, activate microglia, and generate reactive oxygen species to induce autooxidation and dopaminergic neuronal apoptosis. Since no current treatment can cure PD, using a suitable PD animal model to evaluate PD motor symptoms’ treatment efficacy and identify therapeutic targets and drugs are still needed. Hence, the present review focuses on the latest scientific developments in different neurotoxin-induced PD animal models with their mechanisms of pathogenesis and evaluation methods of PD motor symptoms.

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“…Intrastriatal injection of 1-methyl-4-phenylpyridinium (MPP) in rats resulted in the overproduction of free radicals, leading to the production of oxidative stress, decreased levels of dopamine, and behavioral disorders. Oral administration of 100 mg/kg EC before MPP injection significantly prevented dopamine decay and reduced circling behavior related to the damage induced by MPP [ 58 ].…”

Section: Laboratory Studies and Mechanismmentioning

confidence: 99%

Beneficial Effects of Green Tea Catechins on Neurodegenerative Diseases

et al. 2018

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Tea is one of the most consumed beverages in the world. Green tea, black tea, and oolong tea are made from the same plant Camellia sinensis (L.) O. Kuntze. Among them, green tea has been the most extensively studied for beneficial effects on diseases including cancer, obesity, diabetes, and inflammatory and neurodegenerative diseases. Several human observational and intervention studies have found beneficial effects of tea consumption on neurodegenerative impairment, such as cognitive dysfunction and memory loss. These studies supported the basis of tea’s preventive effects of Parkinson’s disease, but few studies have revealed such effects on Alzheimer’s disease. In contrast, several human studies have not reported these favorable effects with regard to tea. This discrepancy may be due to incomplete adjustment of confounding factors, including the method of quantifying consumption, beverage temperature, cigarette smoking, alcohol consumption, and differences in genetic and environmental factors, such as race, sex, age, and lifestyle. Thus, more rigorous human studies are required to understand the neuroprotective effect of tea. A number of laboratory experiments demonstrated the benefits of green tea and green tea catechins (GTCs), such as epigallocatechin gallate (EGCG), and proposed action mechanisms. The targets of GTCs include the abnormal accumulation of fibrous proteins, such as Aβ and α-synuclein, inflammation, elevated expression of pro-apoptotic proteins, and oxidative stress, which are associated with neuronal cell dysfunction and death in the cerebral cortex. Computational molecular docking analysis revealed how EGCG can prevent the accumulation of fibrous proteins. These findings suggest that GTCs have the potential to be used in the prevention and treatment of neurodegenerative diseases and could be useful for the development of new drugs.

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Epicatechin Reduces Striatal MPP⁺-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity

Cited by 12 publications

References 26 publications

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Beneficial Effects of Green Tea Catechins on Neurodegenerative Diseases

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Epicatechin Reduces Striatal MPP+-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity

Cited by 12 publications

References 26 publications

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Beneficial Effects of Green Tea Catechins on Neurodegenerative Diseases

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Product

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Epicatechin Reduces Striatal MPP⁺-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity