Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)
Published: Dec. 19, 2024
Language: Английский
Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)
Published: Dec. 19, 2024
Language: Английский
CNS Neuroscience & Therapeutics, Journal Year: 2025, Volume and Issue: 31(2)
Published: Feb. 1, 2025
ABSTRACT Background Epilepsy, a prevalent neurological disorder, is distinguished by episodic abnormal discharges of neurons within the brain, resulting in transient brain dysfunction. Prior research has identified novel form cell death termed ferroptosis, which intricately linked to initiation and progression epilepsy. It been demonstrated that astaxanthin (AST) can inhibit ferroptosis enhancing activity nuclear factor erythroid 2‐related 2 (Nrf2), thereby providing cytoprotection. Therefore, this study aims investigate whether AST alleviate neuronal epilepsy activating Nrf2/GPX4 pathway, exerting neuroprotective effect. Methods By constructing kainic acid (KA)‐induced mouse model KA‐induced HT22 model, we employed behavioral testing, Western blot analysis, quantitative real‐time reverse transcription qRT‐PCR, ferroptosis‐related assay kits, immunofluorescence staining, other methods. These methodologies were utilized protective effects underlying mechanisms on epileptic mice neurons. Results Our results demonstrate pretreatment alleviates behaviors cognitive impairments mitigates indicators such as lipid peroxidation mitochondrial morphological alterations. This effect appears be mediated activation signaling axis. In vitro studies further revealed confers neuroprotection against death, an abrogated Nrf2 inhibitor. Hence, properties are significantly associated with modulation Nrf2‐mediated corroborated bioinformatics analyses. Conclusion The effectively inhibits both vivo models via pathway. finding suggests holds promise potential therapeutic agent for treatment
Language: Английский
Citations
2Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)
Published: April 15, 2025
Language: Английский
Citations
0International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2762 - 2762
Published: March 19, 2025
Parkinson’s disease (PD) is the second most common progressive neurodegenerative disorder, affecting an increasing number of older adults. Despite extensive research, a definitive cure remains elusive. Eucommia ulmoides Oliv. leaves (EUOL) have been reported to exhibit protective effects on diseases, however, their efficacy, key active constituents, and pharmacological mechanisms are not yet understood. This study aims explore optimal constituents EUOL regarding anti-PD activity its underlying mechanisms. Using zebrafish PD model, we found that 30% ethanol fraction extract (EF) significantly relieved MPTP-induced locomotor impairments, increased length dopaminergic neurons, inhibited loss neuronal vasculature, regulated misexpression autophagy-related genes (α-syn, lc3b, p62, atg7). Assays regulators involved in further verified potential EF against cellular model. Reverse phase protein array (RPPA) analysis revealed exerted by activating 4E-BP1, which was confirmed Western blotting. Phytochemical indicated cryptochlorogenic acid, chlorogenic asperuloside, caffeic asperulosidic acid main components EF. Molecular docking surface plasmon resonance (SPR) exhibited favorable binding interactions with highlighting roles 4E-BP1 this process. Accordingly, these were observed ameliorate PD-like behaviors Overall, constituent EUOL, had considerable ameliorative up-regulating 4E-BP1. suggests could serve as promising candidate for development novel functional foods aimed at supporting treatment.
Language: Английский
Citations
0Parkinson s Disease, Journal Year: 2025, Volume and Issue: 2025(1)
Published: Jan. 1, 2025
Oxidative stress (OS), a condition that occurs when the balance between reactive oxygen species production and antioxidant defense mechanisms is disrupted, has been implicated in pathogenesis of several neurological conditions, including neurodegenerative vascular disorders. Ferroptosis mechanism mediating OS-induced damage, with growing evidence specific involvement both Parkinson's disease (PD) ischemic stroke. Regular physical activity may have an effect by increasing nonenzymatic enzymatic antioxidants. Among biological mediators activity, irisin act as agent capable inducing systemic changes crossing brain-blood barrier. This review aims to describe main role OS pathophysiology PD, highlighting putative emphasizing potential targeting possible shared preventive symptomatic treatment approach.
Language: Английский
Citations
0Antioxidants, Journal Year: 2025, Volume and Issue: 14(4), P. 392 - 392
Published: March 26, 2025
Glycation is a process in which reducing sugars bind to proteins, resulting the formation of advanced glycation end products (AGEs). These AGEs accumulate skin, promote excessive collagen crosslinking, and disrupt extracellular matrix (ECM), impairing normal cellular functions contributing skin aging. To evaluate anti-glycation efficacy lotus stamen extract (LSE), we employed BSA–fructose system high glucose (HG)-induced fibroblast model. The results demonstrated that LSE effectively inhibited also exhibited anti-inflammatory, antioxidative, anti-senescent effects HG-induced human fibroblasts (HSF). Further investigation into mechanism component analysis ethyl acetate (LSEE) led identification 15 flavonoids. indicated these flavonoids are likely primary active constituents LSE. Mechanistic studies revealed GLO1 plays crucial role resistance glycation, LSEE enhanced expression through Nrf2/Keap1 pro-survival pathway, thereby mitigating intracellular AGE production. In summary, its multiple flavonoid components exhibit potent activity present significant potential be developed as natural organic product for cosmetic healthcare applications.
Language: Английский
Citations
0International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 311, P. 143986 - 143986
Published: May 6, 2025
Language: Английский
Citations
0Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)
Published: Dec. 19, 2024
Language: Английский
Citations
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