Much More than Nutrients: The Protective Effects of Nutraceuticals on the Blood–Brain Barrier in Diseases

Nutrients, Год журнала: 2025, Номер 17(5), С. 766 - 766

Опубликована: Фев. 21, 2025

The dysfunction of the blood-brain barrier (BBB) is well described in several diseases, and considered a pathological factor many neurological disorders. This review summarizes most important groups natural compounds, including alkaloids, flavonoids, anthocyanidines, carotenoids, lipids, vitamins that were investigated for their potential protective effects on brain endothelium. penetration these compounds interaction with BBB efflux transporters solute carriers are discussed. cerebrovascular endothelium therapeutic target diseases. In preclinical studies modeling systemic central nervous system nutraceuticals exerted beneficial BBB. vivo, they decreased permeability, edema, astrocyte swelling, morphological changes vessel structure basal lamina. At level endothelial cells, increased cell survival apoptosis. From general functions, angiogenesis levels vasodilating agents demonstrated. elevated integrity by tightened intercellular junctions, expression activity transporters, such as pumps, carriers, metabolic enzymes, shown. Nutraceuticals enhanced antioxidative defense anti-inflammatory at signaling mediating stability activation WNT, PI3K-AKT, NRF2 pathways, inhibition MAPK, JNK, ERK, NF-κB pathways. represent valuable source new potentially molecules to treat diseases protecting

Язык: Английский

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Furanodienone induces apoptosis via regulating the PRDX1/MAPKs/p53/caspases signaling axis through NOX4-derived mitochondrial ROS in colorectal cancer cells

Biochemical Pharmacology, Год журнала: 2024, Номер 227, С. 116456 - 116456

Опубликована: Июль 28, 2024

Furanodienone, a biologically active constituent of sesquiterpenes isolated from Rhizome Curcumae, has been reported to induce apoptosis in human colorectal cancer (CRC) cells by promoting the generation reactive oxygen species (ROS). However, source ROS and how it manipulates CRC remains be elucidated. Herein, we assessed potential role well-known sources intracellular ROS-mitochondrial electron transport chain nicotinamide adenine dinucleotide phosphate oxidases (NOXs), on furanodienone-induced cell death. The results indicated that furanodienone substantially increased levels mitochondrial ROS, which were subsequently eliminated general NOX inhibitor. Specifically, nuclear factor kappa-B (NF-κB) translocation triggered significant rise expression NOX4, an isoform NOXs family, upon treatment. Nevertheless, specific NOX4 inhibitor GLX351322 attenuated production. As result, burst induced suppressed peroxiredoxin1 (PRDX1), redox signaling protein overexpressed cells, through factor-erythroid-2-related 2 (Nrf2)-dependent pathway, thus amplifying mitogen-activated kinases (MAPKs)/p53-mediated apoptotic increasing p-p38, p-JNK levels, as well cleaved caspases -3, -8 -9. In vivo experiments further confirmed anti-proliferative impact PRDX1 following summary, study demonstrated is initiated derived targeted activated downstream MAPKs/p53-mediated caspase-dependent pathway. Our findings may provide novel insights into development adjuvant drugs for treatment therapeutic applications.

Язык: Английский

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Static magnetic field promotes the doxorubicin toxicity effects on osteosarcoma cells

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Апрель 7, 2025

Язык: Английский

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Targeting ferroptosis: a novel pathway in oral, oropharyngeal, hypopharyngeal, and laryngeal cancers

Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 14, 2025

Язык: Английский

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