Опубликована: Янв. 1, 2024
Язык: Английский
Neuroscience, Год журнала: 2025, Номер 569, С. 161 - 183
Опубликована: Фев. 7, 2025
Язык: Английский
Процитировано
1
Pharmaceuticals, Год журнала: 2024, Номер 17(6), С. 701 - 701
Опубликована: Май 28, 2024
Neurodegenerative diseases (Alzheimer’s disease, Parkinson’s Huntington’s and others) cancer, seemingly disparate in their etiology manifestation, exhibit intriguing associations certain cellular molecular processes. Both cancer neurodegenerative involve the deregulation of processes such as apoptosis, proliferation, DNA repair pose a significant global health challenge. Afzelin (kaempferol 3-O-rhamnoside) is flavonoid compound abundant various plant sources. exhibits diverse range biological activities, offering promising prospects for treatment hallmarked by oxidative stress cell death pathways. Its protective potential against also alleviating side effects chemotherapy. This review explores therapeutic implications afzelin, including its capacity to mitigate stress, modulate inflammation, promote regeneration diseases.
Язык: Английский
Процитировано
6
Pharmaceuticals, Год журнала: 2024, Номер 17(11), С. 1480 - 1480
Опубликована: Ноя. 4, 2024
The intricate relationship between hydrogen sulfide (H2S), gut microbiota, and sirtuins (SIRTs) can be seen as a paradigm axis in maintaining cellular homeostasis, modulating oxidative stress, promoting mitochondrial health, which together play pivotal role aging neurodegenerative diseases. H2S, gasotransmitter synthesized endogenously by specific acts potent modulator of function protecting against damage. Through sulfate-reducing bacteria, microbiota influences systemic H2S levels, creating link health metabolic processes. Dysbiosis, or an imbalance microbial populations, alter production, impair function, increase heighten inflammation, all contributing factors diseases such Alzheimer’s Parkinson’s. Sirtuins, particularly SIRT1 SIRT3, are NAD+-dependent deacetylases that regulate biogenesis, antioxidant defense, inflammation. enhances sirtuin activity through post-translational modifications, sulfhydration, activate pathways essential for mitigating damage, reducing longevity. SIRT1, example, deacetylates NF-κB, pro-inflammatory cytokine expression, while SIRT3 modulates key enzymes to improve energy metabolism detoxify reactive oxygen species (ROS). This synergy is profoundly influenced the levels and, turn, impacts activation. microbiota–H2S–sirtuin also regulating neuroinflammation, plays central pathogenesis Pharmacological interventions, including donors sirtuin-activating compounds (STACs), promise these synergistically, providing novel therapeutic approach conditions. suggests diversity optimal have far-reaching effects on brain health.
Язык: Английский
Процитировано
6
Food Chemistry, Год журнала: 2024, Номер 467, С. 142266 - 142266
Опубликована: Ноя. 27, 2024
Язык: Английский
Процитировано
6
Biomolecules, Год журнала: 2024, Номер 14(5), С. 589 - 589
Опубликована: Май 16, 2024
Excitotoxicity is a common pathological process in neurological diseases caused by excess glutamate. The purpose of this study was to evaluate the effect gypenoside XVII (GP-17), monomer, on glutamatergic system. In vitro, rat cortical nerve terminals (synaptosomes), GP-17 dose-dependently decreased glutamate release with an IC50 value 16 μM. removal extracellular Ca2+ or blockade N-and P/Q-type channels and protein kinase A (PKA) abolished inhibitory from synaptosomes. also significantly reduced phosphorylation PKA, SNAP-25, synapsin I vivo model excitotoxicity induced kainic acid (KA), pretreatment prevented seizures rescued neuronal cell injury elevation cortex. expression levels sodium-coupled neutral amino transporter 1, synthesis enzyme glutaminase vesicular 1 but increased level metabolism dehydrogenase cortex KA-treated rats. addition, KA-induced alterations N-methyl-D-aspartate receptor subunits GluN2A GluN2B were pretreatment. decrease cerebral blood flow arginase II expression. These results suggest that (i) GP-17, through suppression N- consequent PKA-mediated SNAP-25 phosphorylation, reduces exocytosis synaptosomes; (ii) has neuroprotective rats regulating synaptic flow.
Язык: Английский
Процитировано
5
Foods, Год журнала: 2024, Номер 13(12), С. 1931 - 1931
Опубликована: Июнь 19, 2024
Over the past decades, there has been a significant increase in burden of neurological diseases, including neurodegenerative disorders, on global scale. This is linked to widespread demographic trend which developed societies are aging, leading an increased proportion elderly individuals and, concurrently, number those afflicted, posing one main public health challenges for coming decades. The complex pathomechanisms diseases and resulting varied symptoms, differ depending disease, environment, lifestyle patients, make searching therapies this group disorders formidable challenge. Currently, most considered incurable. An important aspect fight against prevention may be broadly understood choices, more specifically, what we will focus review, diet. One proposal that help spread diet rich flavonoids. Flavonoids compounds widely found products healthy, such as fruits, vegetables, herbs. Many studies indicated not only neuroprotective effects these but also their ability reverse changes occurring during progression Alzheimer’s, Parkinson’s amyotrophic lateral sclerosis. Here, present groups flavonoids, discussing characteristics mechanisms action. described point functions due strong antioxidant anti-inflammatory effects, accompanied with penetrate blood-brain barrier, well inhibit formation protein aggregates. latter feature, together promoting removal aggregates especially diseases. We discuss therapeutic potential selected flavonoids based vitro studies, impact when included animals (laboratory research) humans (population studies). Thus, review summarizes flavonoids’ actions impacts Therapeutic use future potentially possible depends overcoming key low bioavailability, determining dose, defining flavonoid-rich its negative effects. suggests further research directions address challenges.
Язык: Английский
Процитировано
5
Molecules, Год журнала: 2025, Номер 30(5), С. 1014 - 1014
Опубликована: Фев. 22, 2025
Nuclear receptors such as glucocorticoid (GRs) are transcription factors with prominent regulatory effects on neuroinflammation. Agathisflavone is a biflavonoid that demonstrates neurogenic, neuroprotective, anti-inflammatory, antioxidant, and pro-myelinogenic in vitro. This study investigated whether the control of glial reactivity by agathisflavone mediated GRs. Primary cultures astrocytes microglia were induced to neuroinflammation lipopolysaccharides (LPSs) exposed or not presence absence mifepristone, GR antagonist. The morphology evaluated immunofluorescence against calcium-binding ionized adapter (Iba-1) CD68. astrocyte fibrillary acidic protein (GFAP). inflammatory profile was RT-qPCR. Molecular docking performed characterize interactions. Microglial branching increased response agathisflavone, an effect inhibited mifepristone. CD68 GFAP expression decreased but pro-inflammatory cytokine IL-1β IL-10. increase IL-10 mRNA silico analysis showed binds pocket at receptor. These interactions stronger than dexamethasone, monomer apigenin. results indicate involved inflammation, contributing elucidation molecular mechanisms agathisflavone's nervous system.
Язык: Английский
Процитировано
0
NeuroToxicology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0
Neurochemistry International, Год журнала: 2024, Номер 180, С. 105859 - 105859
Опубликована: Сен. 10, 2024
Язык: Английский
Процитировано
2
International Journal of Pharmaceutics, Год журнала: 2024, Номер unknown, С. 125135 - 125135
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
2