Mitochondrial-Targeted Ratiometric Near-Infrared Fluorescence Probe for Monitoring Nitric Oxide in Rheumatoid Arthritis

Journal of Medicinal Chemistry, Год журнала: 2024, Номер 67(5), С. 4026 - 4035

Опубликована: Фев. 15, 2024

Rheumatoid arthritis (RA) is a destructive autoimmune disease, where nitric oxide (NO) closely implicated in the inflammatory processes of RA. Therefore, direct visualization NO essential to assess pathological changes Herein, mitochondrial-targeted near-infrared ratiometric fluorescent probe (NFL-NH2), based on intramolecular charge transfer effect, was synthesized and applied monitor content early Specially, NFL-NH2 showed 44-fold intensity ratio (I705/I780) response toward with detection limit 0.536 nM, enabling qualitative quantitative analysis NO. Additionally, can accurately target mitochondria sensitively detect exogenous endogenous RAW 264.7 cells. Notably, vivo RA monitoring assays demonstrated that rapidly levels associated damage degree mice models by fluorescence imaging. These results validate holds significant potential for diagnosing NO-mediated diseases.

Язык: Английский

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Metabolomics provide novel insights into the settlement and metamorphosis of the scyphozoan jellyfish Aurelia coerulea

Journal of Oceanology and Limnology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 2, 2025

Язык: Английский

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Aminoguanidine hemisulfate improves mitochondrial autophagy, oxidative stress, and muscle force in Duchenne muscular dystrophy via the AKT/FOXO1 pathway in mdx mice

Skeletal Muscle, Год журнала: 2025, Номер 15(1)

Опубликована: Янв. 13, 2025

Duchenne muscular dystrophy (DMD) is a prevalent, fatal degenerative muscle disease with no effective treatments. Mdx mouse model of DMD exhibits impaired performance, oxidative stress, and dysfunctional autophagy. Although antioxidant treatments may improve the mdx phenotype, precise molecular mechanisms remain unclear. This study investigates effects aminoguanidine hemisulfate (AGH), an inhibitor reactive oxygen species (ROS), on mitochondrial autophagy, force in mice. Male wild-type (WT) mice were divided into three groups: WT, mdx, AGH-treated (40 mg/kg intraperitoneally for two weeks) at 6 weeks age. Gene expression, western blotting, H&E staining, immunofluorescence, ROS assays, TUNEL apoptosis, glutathione activity, measurements performed. Statistical comparisons used one-way ANOVA. AGH treatment significantly reduced protein levels LC3, p62 mice, indicating improved autophagy activity ability to clear damaged mitochondria. restored expression mitophagy-related genes Pink1 Parkin increased Mfn1, rebalancing dynamics. It also Pgc1α mtTFA levels, promoting biogenesis. reduced, higher Prdx3 MnSOD improving defenses. normalized GSSG/GSH ratio decreased reductase peroxidase activities, further redox homeostasis. Additionally, shown by fewer TUNEL-positive cells lower caspase-3 expression. Histological analysis revealed damage embryonic neonatal myosin-expressing fibers. altered fiber composition, decreasing MyH7 while increasing MyH4 MyH2. Muscle significantly, greater twitch tetanic forces. Mechanistically, modulated AKT/FOXO1 pathway, myogenin Foxo1 MyoD. composition via collectively We propose as potential therapeutic strategy related disorders.

Язык: Английский

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BPA-induced disruption of muscle development and larval metamorphosis in the mussel Mytilus coruscus

Aquatic Toxicology, Год журнала: 2025, Номер unknown, С. 107368 - 107368

Опубликована: Апрель 1, 2025

Язык: Английский

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