OXIDATIVE STRESS AS A MOLECULAR BASIS FOR NEURODEGENERATIVE DISEASES AND ANTIOXIDANT THERAPY PATHWAYS DOI Open Access
З. И. Микашинович, Н. Р. Телесманич, Olga Smirnova

и другие.

Scientific Notes of V I Vernadsky Crimean Federal University Biology Chemistry, Год журнала: 2024, Номер 10(3), С. 106 - 127

Опубликована: Дек. 12, 2024

The review presents the results of clinical and experimental studies demonstrating pathogenetic role oxidative stress in genesis neurodegenerative diseases (NDD), obtained using a complex clinical, laboratory instrumental methods that reveal antioxidants NDD. In process preparing materials, sources from international domestic databases were used: Scopus, Web Science, Pub Medline, RSCI, mainly over past 15 years (2010–2024). Diseases nervous system differ etiology symptoms have common mechanisms associated with damage to biomolecules: improper protein stacking, their aggregation, violation pro- antioxidant balance. Increased formation reactive oxygen species (ROS) induces mitoptosis, apoptosis, ferroptosis, factors lead impaired functional activity neuron structural units as main element system. Given complexity pathogenesis NDZ, promising methodological approach is calculate leading pathogenesis. Undoubtedly, this makes it possible standardize diagnosis therapy, subsequently create recommendations. purpose work was analyze participants key stages inflammatory underlying NDZ. Despite fact there currently no unambiguous recognition effectiveness nevertheless, use can be considered most important link neuroprotection, which has justification. Metabolic correction NDH divided into 3 groups: natural antioxidants, then endogenous oxidants coming food, 3rd group includes drugs combination therapy immunotherapy. Mexidol selenoproteins antihypoxic effects, are realized at both neuronal vascular levels. Prospects for development effective metabolic restoration mitochondrial dysfunction. Synchronization processes functioning structures will ensure neurogeneration, slow down increase life expectancy. FDA-approved such acetylcholinesterase inhibitors (donepezil, rivastigmine), well levodopa treatment PD, cross blood-brain barrier restore dopamine levels substantia nigra, only alleviate progression several years. New therapeutic approaches aimed neuroregeneration, i.e. damaged through immunomodulation, inhibition aggregates, disaggregation improperly folded proteins induction autophagy, give hope degeneration affected neurons may down, recovery rate expectancy increase. Due nature NDT, multi-purpose recommended, additional positive effects.

Язык: Английский

Unrevealing the molecular mechanisms of MPTP-induced Parkinson’s in experimental animals DOI
Somnath Mondal, Sayeed Mohammed Firdous

Medicinal Chemistry Research, Год журнала: 2025, Номер unknown

Опубликована: Апрель 14, 2025

Язык: Английский

Процитировано

0
Natural Compounds That Activate the KEAP1/Nrf2 Signaling Pathway as Potential New Drugs in the Treatment of Idiopathic Parkinson’s Disease DOI Creative Commons
Sandro Huenchuguala, Juan Segura‐Aguilar

Antioxidants, Год журнала: 2024, Номер 13(9), С. 1125 - 1125

Опубликована: Сен. 18, 2024

Recently, a single-neuron degeneration model has been proposed to understand the development of idiopathic Parkinson's disease based on (i) extremely slow degenerative process before onset motor symptoms and during progression (ii) fact that it is triggered by an endogenous neurotoxin does not have expansive character, limiting its neurotoxic effect single neuromelanin-containing dopaminergic neurons. It aminochrome triggers neurodegenerative in triggering mitochondrial dysfunction, oxidative stress, neuroinflammation, dysfunction both lysosomal proteasomal protein degradation, endoplasmic reticulum stress formation alpha-synuclein oligomers. Aminochrome rapidly reduced flavoenzymes and/or forms adducts with proteins, which implies impossible for propagative neighboring Interestingly, enzymes DT-diaphorase glutathione transferase M2-2 prevent effects aminochrome. Natural compounds present fruits, vegetables other plant products shown activate KEAP1/Nrf2 signaling pathway increasing expression antioxidant including transferase. This review analyzes possibility searching natural increase through activation pathway.

Язык: Английский

Процитировано

1
L-Theanine Effectively Protects Against Copper-Facilitated Dopamine Oxidation: Implication for Relieving Dopamine Overflow-Associated Neurotoxicities DOI
Fu‐Ming Wang, Xiaoyu Huang, Wenping Wang

и другие.

Molecular Neurobiology, Год журнала: 2024, Номер 62(4), С. 4993 - 5005

Опубликована: Ноя. 5, 2024

Язык: Английский

Процитировано

1
Glutathione S-transferase: A keystone in Parkinson's disease pathogenesis and therapy DOI

Pratyush Padhan,

Simran Simran,

Neeraj Kumar

и другие.

Molecular and Cellular Neuroscience, Год журнала: 2024, Номер unknown, С. 103981 - 103981

Опубликована: Дек. 1, 2024

Язык: Английский

Процитировано

1
Oxyphylla A exerts antiparkinsonian effects by ameliorating 6-OHDA-induced mitochondrial dysfunction and dyskinesia in vitro and in vivo DOI
Min Shao, Chen Zhao,

Zhijian Pan

и другие.

Chemico-Biological Interactions, Год журнала: 2024, Номер 403, С. 111224 - 111224

Опубликована: Сен. 3, 2024

Язык: Английский

Процитировано

0
Coumarin-chalcone derivatives as dual NLRP1 and NLRP3 inflammasome inhibitors targeting oxidative stress and inflammation in neurotoxin-induced HMC3 and BE(2)-M17 cell models of Parkinson's disease DOI Creative Commons
Te‐Hsien Lin, Ya‐Jen Chiu, Chih‐Hsin Lin

и другие.

Frontiers in Aging Neuroscience, Год журнала: 2024, Номер 16

Опубликована: Окт. 1, 2024

Background In Parkinson's disease (PD) brains, microglia are activated to release inflammatory factors induce the production of reactive oxygen species (ROS) in neuron, and vice versa. Moreover, neuroinflammation its synergistic interaction with oxidative stress contribute pathogenesis PD. Methods this study, we investigated whether in-house synthetic coumarin-chalcone derivatives protect human HMC3 neuroblastoma BE(2)-M17 cells against 1-methyl-4-phenyl pyridinium (MPP + )-induced associated neuronal damage. Results Treatment MPP decreased cell viability as well increased mediators including cytokines nitric oxide culture medium, enhanced expression microglial activation markers CD68 MHCII cells. The protein levels NLRP3, CASP1, iNOS, IL-1β, IL-6, TNF-α were also -stimulated Among four tested compounds, LM-016, LM-021, LM-036 at 10 μM counteracted action addition, LM-021 viability, reduced lactate dehydrogenase release, ameliorated cellular ROS production, caspase-1, caspase-3 caspase-6 activities, promoted neurite outgrowth -treated These protective effects mediated by down-regulating NLRP1, TNF-α, up-regulating antioxidative NRF2, NQO1, GCLC, PGC-1α, neuroprotective CREB, BDNF, BCL2. Conclusion study results strengthen involvement PD pathogenic mechanisms, indicate potential use dual inflammasome inhibitors treating both NLRP1- NLRP3-associated

Язык: Английский

Процитировано

0
OXIDATIVE STRESS AS A MOLECULAR BASIS FOR NEURODEGENERATIVE DISEASES AND ANTIOXIDANT THERAPY PATHWAYS DOI Open Access
З. И. Микашинович, Н. Р. Телесманич, Olga Smirnova

и другие.

Scientific Notes of V I Vernadsky Crimean Federal University Biology Chemistry, Год журнала: 2024, Номер 10(3), С. 106 - 127

Опубликована: Дек. 12, 2024

The review presents the results of clinical and experimental studies demonstrating pathogenetic role oxidative stress in genesis neurodegenerative diseases (NDD), obtained using a complex clinical, laboratory instrumental methods that reveal antioxidants NDD. In process preparing materials, sources from international domestic databases were used: Scopus, Web Science, Pub Medline, RSCI, mainly over past 15 years (2010–2024). Diseases nervous system differ etiology symptoms have common mechanisms associated with damage to biomolecules: improper protein stacking, their aggregation, violation pro- antioxidant balance. Increased formation reactive oxygen species (ROS) induces mitoptosis, apoptosis, ferroptosis, factors lead impaired functional activity neuron structural units as main element system. Given complexity pathogenesis NDZ, promising methodological approach is calculate leading pathogenesis. Undoubtedly, this makes it possible standardize diagnosis therapy, subsequently create recommendations. purpose work was analyze participants key stages inflammatory underlying NDZ. Despite fact there currently no unambiguous recognition effectiveness nevertheless, use can be considered most important link neuroprotection, which has justification. Metabolic correction NDH divided into 3 groups: natural antioxidants, then endogenous oxidants coming food, 3rd group includes drugs combination therapy immunotherapy. Mexidol selenoproteins antihypoxic effects, are realized at both neuronal vascular levels. Prospects for development effective metabolic restoration mitochondrial dysfunction. Synchronization processes functioning structures will ensure neurogeneration, slow down increase life expectancy. FDA-approved such acetylcholinesterase inhibitors (donepezil, rivastigmine), well levodopa treatment PD, cross blood-brain barrier restore dopamine levels substantia nigra, only alleviate progression several years. New therapeutic approaches aimed neuroregeneration, i.e. damaged through immunomodulation, inhibition aggregates, disaggregation improperly folded proteins induction autophagy, give hope degeneration affected neurons may down, recovery rate expectancy increase. Due nature NDT, multi-purpose recommended, additional positive effects.

Язык: Английский

Процитировано

0