Neuroprotective effects of morroniside from Cornus officinalis sieb. Et zucc against Parkinson’s disease via inhibiting oxidative stress and ferroptosis

BMC Complementary Medicine and Therapies, Journal Year: 2023, Volume and Issue: 23(1)

Published: July 1, 2023

Parkinson's disease (PD) is the second most common neurodegenera-tive disorder after Alzheimer accompanied by death of dopaminergic neurons and brain nigrostriatal mitochondrial damage in elderly population. The features include tremor, rigidity, postural instability, motor retardation. pathogenesis complex, abnormal lipid metabolism resulting ferroptosis due to excessive accumulation free radicals from oxidative stress substantia nigra was thought be one factors causing disease. Morroniside has been reported have significant neuroprotective effects, although it not studied PD. Therefore, this study focused on determining effects morroniside (25, 50, 100 mg/kg) 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg)-induced mice models PD explored 1-methyl-4-phenylpyridinium MPP+-induced PC12 cells. restored impaired function while reducing neuronal injury. activation nuclear factor erythroid 2-related 2/antioxidant response elements (Nrf2/ARE) promoted antioxidation, content agent glutathione (GSH) increased, level metabolite malondialdehyde (MDA) decreased. Notably, inhibited cells, reduced iron levels, upregulated expression iron-regulated proteins peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), ferritin heavy chain 1 (FTH-1), ferroportin (FPN). More importantly, repaired damage, respiratory chain, production reactive oxygen species (ROS). These data indicated that could activate Nrf2/ARE signaling pathway increase antioxidant capacity, thereby inhibiting protecting

Language: Английский

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The role and intervention of mitochondrial metabolism in osteoarthritis

Molecular and Cellular Biochemistry, Journal Year: 2023, Volume and Issue: 479(6), P. 1513 - 1524

Published: July 24, 2023

Abstract Osteoarthritis (OA), a prevalent degenerative joint disease, affects substantial global population. Despite the elusive etiology of OA, recent investigations have implicated mitochondrial dysfunction as significant factor in disease pathogenesis. Mitochondria, pivotal cellular organelles accountable for energy production, exert essential roles metabolism. Hence, can broad-ranging effects on various processes OA development. This comprehensive review aims to provide an overview metabolic alterations occurring and elucidate diverse mechanisms through which contribute These encompass heightened oxidative stress inflammation, perturbed chondrocyte metabolism, compromised autophagy. Furthermore, this will explore potential interventions targeting metabolism means impede or decelerate progression OA. In summary, offers understanding involvement underscores prospective intervention strategies.

Language: Английский

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Focusing on mitochondria in the brain: from biology to therapeutics

Translational Neurodegeneration, Journal Year: 2024, Volume and Issue: 13(1)

Published: April 17, 2024

Abstract Mitochondria have multiple functions such as supplying energy, regulating the redox status, and producing proteins encoded by an independent genome. They are closely related to physiology pathology of many organs tissues, among which brain is particularly prominent. The demands 20% resting metabolic rate holds highly active mitochondrial activities. Considerable research shows that mitochondria function, while defects induce or exacerbate in brain. In this review, we provide comprehensive advances biology involved functions, well mitochondria-dependent cellular events pathology. Furthermore, various perspectives explored better identify roles neurological diseases neurophenotypes diseases. Finally, therapies discussed. Mitochondrial-targeting therapeutics showing great potentials treatment

Language: Английский

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Recent development of mitochondrial metabolism and dysfunction in osteoarthritis

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 13, 2025

Osteoarthritis is a degenerative joint disorder characterized by cartilage degradation, synovial inflammation, and altered subchondral bone structure. Recent insights have identified mitochondrial dysfunction as pivotal factor in OA pathogenesis, contributing to chondrocyte apoptosis, oxidative stress, extracellular matrix degradation. Disruptions dynamics, including impaired biogenesis, mitophagy, metabolic shifts from phosphorylation glycolysis, exacerbate damage promoting the production of reactive oxygen species matrix-degrading enzymes such ADAMTS MMPs. This review explores molecular mechanisms underlying OA, emphasizing its role homeostasis inflammation. Furthermore, it highlights emerging therapeutic strategies targeting pathways, antioxidants, mitophagy enhancers, modulators, potential interventions mitigate disease progression, which offer promising avenues for advancing personalized disease-modifying treatments OA.

Language: Английский

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Structure of mitochondrial pyruvate carrier and its inhibition mechanism

Nature, Journal Year: 2025, Volume and Issue: unknown

Published: March 5, 2025

Language: Английский

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