Targeting natural antioxidant polyphenols to protect neuroinflammation and neurodegenerative diseases: a comprehensive review

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Янв. 24, 2025

Polyphenols, naturally occurring phytonutrients found in plant-based foods, have attracted significant attention for their potential therapeutic effects neurological diseases and neuroinflammation. These compounds possess diverse neuroprotective capabilities, including antioxidant, anti-inflammatory, anti-amyloid properties, which contribute to mitigating the progression of neurodegenerative conditions such as Alzheimer's Disease (AD), Parkinson's (PD), Dementia, Multiple Sclerosis (MS), Stroke, Huntington's (HD). Polyphenols been extensively studied ability regulate inflammatory responses by modulating activity pro-inflammatory genes influencing signal transduction pathways, thereby reducing neuroinflammation neuronal death. Additionally, polyphenols shown promise various cellular signaling pathways associated with viability, synaptic plasticity, cognitive function. Epidemiological clinical studies highlight polyphenol-rich diets decrease risk alleviate symptoms disorders Furthermore, demonstrated through regulation key Akt, Nrf2, STAT, MAPK, play critical roles neuroprotection body's immune response. This review emphasizes growing body evidence supporting combating neurodegeneration neuroinflammation, well enhancing brain health. Despite substantial promising hypotheses, further research investigations are necessary fully understand role establish them advanced targets age-related neuroinflammatory conditions.

Язык: Английский

---

Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies

Biomedicines, Год журнала: 2025, Номер 13(2), С. 327 - 327

Опубликована: Янв. 31, 2025

Neurodegenerative disease (ND) refers to the progressive loss and morphological abnormalities of neurons in central nervous system (CNS) or peripheral (PNS). Examples neurodegenerative diseases include Alzheimer's (AD), Parkinson's (PD), amyotrophic lateral sclerosis (ALS). Recent studies have shown that mitochondria play a broad role cell signaling, immune response, metabolic regulation. For example, mitochondrial dysfunction is closely associated with onset progression variety diseases, including ND, cardiovascular diabetes, cancer. The energy metabolism, imbalance dynamics, abnormal mitophagy can lead homeostasis, which induce pathological reactions such as oxidative stress, apoptosis, inflammation, damage system, participate occurrence development degenerative AD, PD, ALS. In this paper, latest research progress subject detailed. mechanisms mitophagy-mediated ND are reviewed from perspectives β-amyloid (Aβ) accumulation, dopamine neuron damage, superoxide dismutase 1 (SOD1) mutation. Based on mechanism research, new ideas methods for treatment prevention proposed.

Язык: Английский

---

Physical Exercise-Induced Activation of NRF2 and BDNF as a Promising Strategy for Ferroptosis Regulation in Parkinson’s Disease

Neurochemical Research, Год журнала: 2024, Номер 49(7), С. 1643 - 1654

Опубликована: Май 24, 2024

Язык: Английский

---

Ferroptosis in Neurons: A Bibliometric Analysis of Research Trends, Key Contributions, and Emerging Directions

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Янв. 17, 2025

Background Neurons are the fundamental structural and functional units of nervous system, serving as core cells for information transmission regulation. They closely associated with various neurological diseases. Recent studies have shown significant advancements in research on ferroptosis neurons; however, there has been a lack bibliometric analysis this field. This study aims to provide comprehensive overview knowledge structure related neurons through methods, identify current trends hotspots, predict potential future directions. Methods We conducted search publications from 2014 2024 Web Science Core Collection (WoSCC) database. Bibliometric methods were employed analyze authors, institutions, countries, journals, references using VOSviewer, CiteSpace, R package "bibliometrix". Results included 685 articles 50 China United States being leading contributors. The number year-on-year increase. primary institutions Central South University, Harbin Medical University Melbourne. Free Radical Biology Medicine is most popular journal field, while Cell highest citation count. A total 4,673 authors contributed research, David Devos Ashley I. Bush having publications, Scott J. Dixon had co-citations. Keyword revealed that molecular mechanisms its application diseases focuses Conclusion first summarizing developments neurons. outlines predicts global hotspots trends, providing valuable scholars studying ferroptosis.

Язык: Английский

---

Therapeutic Effects of Natural Products in the Treatment of Chronic Diseases: The Role in Regulating KEAP1–NRF2 Pathway

The American Journal of Chinese Medicine, Год журнала: 2025, Номер unknown, С. 1 - 30

Опубликована: Янв. 29, 2025

Oxidative stress represents a pivotal mechanism in the pathogenesis of numerous chronic diseases. The Kelch-like ECH-associated protein 1–transcription factor NF-E2 p45-related 2 (KEAP1–NRF2) pathway plays crucial role maintaining redox homeostasis and regulating multitude biological processes such as inflammation, homeostasis, metabolic homeostasis. In this paper, we present findings recent studies on KEAP1–NRF2 pathway, which have revealed that it is aberrantly regulated induces oxidative injury variety diseases neurodegenerative diseases, cardiovascular respiratory digestive cancer. Given evidence, targeting highly promising avenue for developing therapeutic strategies thus development appropriate based NRF2 has emerged significant area research interest. This paper highlights an overview current to modulate KEAP1–NRF2, well advances use natural compounds traditional Chinese medicine, with view providing meaningful guidelines drug discovery KEAP1–NRF2. Additionally, discusses challenges associated harnessing target.

Язык: Английский

---

Gallic acid protects intervertebral disc cells from ferroptosis and alleviates intervertebral disc degeneration by regulating key factors of oxidative stress

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Фев. 3, 2025

Background Intervertebral disc degeneration (IDD) is a chronic degenerative disease and one of the main causes low back pain (LBP). Currently, there no effective treatment. Ferroptosis cell-regulated process that depends on iron deposition lipid peroxidation. Inhibiting ferroptosis in nucleus pulposus cells considered potential strategy for treatment IDD. Gallic acid (GA) naturally present variety plants has anti-inflammatory, antioxidant analgesic effects. It been shown to alleviate ferroptosis. However, role GA IDD remains unclear. Methods This study explored pathological mechanism relation ferroptosis: (1) identify ferroptosis-related targets using network pharmacology molecular docking technology, (2) evaluate therapeutic effect an rat model changes targets, (3) investigate oxidative stress peroxidation products NP after intervention, (4) proteins ions mitochondria intervention. Results Experimental results confirmed can treat by reducing degradation extracellular matrix (ECM) also mitigate (NP) cells. Conclusion The alleviation may be closely associated with key P53 NRF2.

Язык: Английский

---

Lycium ruthenicum anthocyanins alleviate acrylamide-induced neurotoxicity in SH-SY5Y cells by mitigating ferroptosis via the Nrf2/GPX4 signaling pathway

Food Bioscience, Год журнала: 2025, Номер unknown, С. 106415 - 106415

Опубликована: Март 1, 2025

Язык: Английский

---

Ferroptosis in NAFLD: insights and the therapeutic potential of exercise

Frontiers in Medicine, Год журнала: 2025, Номер 12

Опубликована: Март 26, 2025

Ferroptosis, a distinct form of non-apoptotic cell death driven by iron accumulation, has garnered significant attention in recent years. Emerging evidence suggests that ferroptosis hepatocytes may serve as pivotal trigger the pathogenesis non-alcoholic fatty liver disease (NAFLD). Importantly, inhibiting shown promising potential slowing progression NAFLD. Concurrently, exercise, cornerstone prevention and management chronic diseases, plays critical role regulating progression. As such, modulation through exercise represents avenue for developing innovative therapeutic strategies. This review aims to systematically elucidate conceptual framework molecular mechanisms underlying ferroptosis, with particular emphasis on its pathophysiological We have summarized effects regulation multiple mechanisms, including upregulation antioxidant defense systems via activation NRF2, GPX4, SLC7A11 signaling pathways; metabolism FPN-mediated homeostasis regulation. These findings not only provide valuable insights into basis exercise-induced protection against ferroptosis-mediated cellular damage but also offer novel perspectives future investigations exercise-based interventions NAFLD management. work thereby contributes advancement strategies field metabolic diseases.

Язык: Английский

---

METTL14-Mediated m6A Modification of TUG1 Represses Ferroptosis in Alzheimer's Disease via Inhibiting GDF15 Ubiquitination

Frontiers in Bioscience-Landmark, Год журнала: 2024, Номер 29(8)

Опубликована: Авг. 21, 2024

Background: Alzheimer’s disease (AD) is a neurodegenerative that remains serious global health issue. Ferroptosis has been recognized as vital driver of pathological progression AD. However, the detailed regulatory mechanisms ferroptosis during AD remain unclear. This study aimed to explore role and mechanism methyltransferase like 14 (METTL14) in models. Methods: Serum samples were collected from 18 patients healthy volunteers evaluate clinical correlation. Scopolamine-treated mice Aβ1–42-stimulated SH-SY5Y cells served vivo vitro models was detected by reactive oxygen species (ROS), Fe2+, total iron levels, ferroptosis-related proteins glutathione peroxidase 4 (GPX4) solute carrier family 7 member 11 (SLC7A11). Cell viability analyzed 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay. The N6-methyladenosine (m6A) modification RNA methylation quantification kit methylated immunoprecipitation sequencing-quantitative real-time polymerase chain reaction (MeRIP-qPCR). Molecular investigated pull-down, (RIP), co-immunoprecipitation (Co-IP) assays. Cognitive disorder measured Morris water maze test. Results: METTL14 down-regulated, while lncRNA taurine upregulated gene 1 (TUG1) up-regulated experimental Functional experiments demonstrated overexpression or TUG1 silencing effectively attenuated Aβ1–42-induced neurotoxicity cells. Mechanistically, METTL14-mediated m6A reduced stability TUG1. Moreover, promoted ubiquitination degradation growth differentiation factor 15 (GDF15) directly interacted with Smad ubiquitin (SMURF1), which consequently inactivated nuclear erythroid 2-related 2 (NRF2). Rescue indicated GDF15 depletion reversed sh-TUG1-mediated protection against neurotoxicity. Finally, Mettl14 repressed ameliorate cognitive via modulating Tug1/Gdf15/Nrf2 pathway vivo. Conclusion: inhibited development activate GDF15/NRF2 axis, providing novel therapeutic target for

Язык: Английский

---

Redox chemical delivery system: an innovative strategy for the treatment of neurodegenerative diseases

Expert Opinion on Drug Delivery, Год журнала: 2025, Номер unknown

Опубликована: Апрель 5, 2025

It is anticipated that the prevalence of illnesses affecting central nervous system (CNS) will rise significantly due to longer lifespans and changing demography. Age-related decline in brain function neuronal death are features neurodegenerative disorders, such as Parkinson's disease, Alzheimer's Huntington's amyotrophic lateral sclerosis, which provide formidable treatment challenges. Because most therapeutic drugs cannot pass across blood-brain barrier (BBB) reach brain, there still few alternatives available despite a great deal research. This study explores role redox chemical delivery systems CNS drug addresses challenges associated with disease (ND). Redox Chemical Delivery System offers promising approach enhancing leveraging reactions facilitate transport agents BBB. Through optimization medication pathways this technology has potential greatly improve ND. As our understanding biological underpinnings ND deepens, for effective interventions increases. Refining strategies, RCDS, essential advancing therapies from research clinical practice. These advancements could transform management ND, improving both efficacy patient outcomes.

Язык: Английский

---