Elsevier eBooks, Год журнала: 2024, Номер unknown, С. 285 - 304
Опубликована: Ноя. 29, 2024
Neurotherapeutics, Год журнала: 2024, Номер 21(4), С. e00355 - e00355
Опубликована: Апрель 4, 2024
Mitochondria are essential organelles for cell survival that manage the cellular energy supply by producing ATP. Mitochondrial dysfunction is associated with various human diseases, including metabolic syndromes, aging, and neurodegenerative diseases. Among diseases related to mitochondrial dysfunction, Parkinson's disease (PD) second most common characterized dopaminergic neuronal loss neuroinflammation. Recently, it was reported transfer between cells occurred naturally exogenous transplantation beneficial treating dysfunction. The current study aimed investigate therapeutic effect of on PD in vitro vivo. results showed PN-101 mitochondria isolated from mesenchymal stem exhibited a neuroprotective against 1-methyl-4-phenylpyridinium, 6-hydroxydopamine rotenone ameliorated brains C57BL/6J mice injected 30 mg/kg methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intraperitoneally. In addition, anti-inflammatory effects reducing expression pro-inflammatory cytokines microglial suppressing activation striatum. Furthermore, intravenous treatment behavioral improvements during pole test rotarod MPTP-induced mice. These dual neuroprotection anti-neuroinflammation support potential as novel strategy PD.
Язык: Английский
Процитировано
10
Small, Год журнала: 2024, Номер 20(29)
Опубликована: Фев. 22, 2024
Parkinson's disease (PD) is currently the second most incurable central neurodegenerative resulting from various pathogenesis. As "energy factory" of cells, mitochondria play an extremely important role in supporting neuronal signal transmission and other physiological activities. Mitochondrial dysfunction can cause accelerate occurrence progression PD. How to effectively prevent suppress mitochondrial disorders a key strategy for treatment PD root. Therefore, emerging mitochondria-targeted therapy has attracted considerable interest. Herein, relationship between PD, causes results dysfunction, major strategies ameliorating treat are systematically reviewed. The study also prospects main challenges
Язык: Английский
Процитировано
8
Brain Research, Год журнала: 2025, Номер unknown, С. 149540 - 149540
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0
Journal of Biochemical and Molecular Toxicology, Год журнала: 2024, Номер 38(5)
Опубликована: Апрель 17, 2024
Abstract Parkinson's disease (PD) is a neurodegenerative featured by progressive loss of nigrostriatal dopaminergic neurons, the etiology which associated with existence neuroinflammatory response and oxidative stress. Vincamine an indole alkaloid that was reported to exhibit potent anti‐inflammatory antioxidant properties in many central and/or peripheral diseases. Nevertheless, specific role vincamine PD development remains unknown. In our study, neuron determined through immunohistochemistry staining western blot analysis tyrosine hydroxylase (TH) expression substantia nigra (SN) mice. Reactive oxygen species (ROS) production malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) levels were detected DHE commercially available kits assess Pro‐inflammatory cytokine (TNF‐α, IL‐1β, IL‐6) SN measured via RT‐qPCR analysis. Microglial astrocyte activation examined immunofluorescence Iba‐1 (microglia marker) GFAP (astrocyte SN. The regulation on NF‐κB Nrf2/HO‐1 pathway estimated Our results showed treatment decreased TNF‐α, IL‐6 mRNA protein levels, reduced expression, ROS MDA level, increased SOD activity GSH level Mechanically, repressed phosphorylation p65, IKKβ, IκBα but enhanced Nrf2 HO‐1 Collectively, plays neuroprotective mouse models alleviating neuroinflammation damage suppressing activating pathway.
Язык: Английский
Процитировано
4
International Immunopharmacology, Год журнала: 2024, Номер 142, С. 113015 - 113015
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
4
Metabolic Brain Disease, Год журнала: 2025, Номер 40(2)
Опубликована: Фев. 11, 2025
Язык: Английский
Процитировано
0
Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown
Опубликована: Март 31, 2025
Abstract Neurodegenerative disorders present significant challenges to modern medicine because of their complex etiology, pathogenesis, and progressive nature, which complicate practical treatment approaches. Mitochondrial dysfunction is an important contributor the pathophysiology various neurodegenerative illnesses, including Alzheimer’s disease (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS). This review paper examines current literature highlighting multifaceted functions mitochondria, energy production, calcium signaling, apoptosis regulation, mitochondrial biogenesis, dynamics, axonal transport, endoplasmic reticulum–mitochondrial interactions, mitophagy, proteostasis, crucial involvement in neuronal health. The emphasizes increasing recognition as a critical factor progression disorders, marking shift from traditional symptom management innovative mitochondrial-based therapies. By discussing mechanisms, quality control (MQC) processes impact oxidative stress, this highlights need for novel therapeutic strategies restore function, protect connections integrity, slow progression. comprehensive aims provide insights into potential interventions that could transform landscape diseases, addressing symptoms underlying pathophysiological changes.
Язык: Английский
Процитировано
0
Free Radical Biology and Medicine, Год журнала: 2024, Номер 215, С. 2 - 13
Опубликована: Фев. 22, 2024
Язык: Английский
Процитировано
3
Journal of Muscle Research and Cell Motility, Год журнала: 2024, Номер 45(4), С. 233 - 251
Опубликована: Июнь 1, 2024
Язык: Английский
Процитировано
3
Ageing Research Reviews, Год журнала: 2024, Номер 100, С. 102469 - 102469
Опубликована: Авг. 25, 2024
Язык: Английский
Процитировано
3