Therapeutic potential of 1,3,4-oxadiazole derivative in EAE-induced optic neuritis.

Oxytocin ameliorates cardiac hypertrophy by inhibiting mitochondrial dysfunction and pyroptosis via AMPK/PGC-1α /TFAM pathway.

A mitochondria-targeted "turn-on" near-infrared fluorescent probe for imaging protein Sulfenic acids in live cells under oxidative stress.

Dapagliflozin ameliorates myocardial ischemia/reperfusion injury by modulating EGFR signaling and targeting NCOA4-mediated ferritinophagy.

New co-drugs of O-demethylvenlafaxine and NSAIDs exert antidepressant effects by alleviating inflammation, oxidative stress, and increasing neurotransmitter.

Structural characterization and hypoglycemic mechanisms of a Hericium coralloides heteropolysaccharide (HCP-2b) via gut microbiota modulation and PI3K/Akt signaling.

Nano-delivery system of milk-derived exosomes loaded with Forsythiaside A: Studies on bovine mammary epithelial cells and mastitis induced mice.

Tribulus terrestris L. extract alleviates diabetic nephropathy through regulation of oxidative stress and inflammation: insights from in silico, in vivo and LC-MS/MS-based metabolite profiling studies.

Integrated metabolomics and proteomics analysis elucidated the therapeutic effect of Huangkui Capsule on tacrolimus-induced chronic nephrotoxicity in rats.

Anti-oxidant, anti-estrogenic and anti-inflammatory activities of the UHPLC fingerprinted Acacia seyal Delile (Mimosaceae) extracts: possible anticancer modes of action.

SQSTM1/p62 is a master regulator of the autophagic and ubiquitination pathways of protein degradation and the antioxidant response. p62 functions in these pathways via reversible assembly and sequestration of additional factors into cytoplasmic phase-separated structures termed p62 bodies. The physiological roles of p62 in these various pathways depend on numerous mechanisms for regulating p62 body formation and dynamics that are incompletely understood. Here, we identify a new mechanism for regulation of p62 oligomerization and incorporation into p62 bodies by SHKBP1, a cullin-3 E3 ubiquitin ligase adaptor, that is independent of its potential functions in ubiquitination. We map an SHKBP1-p62 protein-protein interaction outside of p62 bodies that limits p62 assembly into p62 bodies and affects the antioxidant response involving sequestration of Keap1 and nuclear translocation of Nrf2. These studies provide a non-ubiquitination-based mechanism for an E3 ligase adaptor in regulating p62 body formation and cellular responses to oxidative stress.

Is oxidative stress in the brain correlated with plasma markers of oxidative stress?

Oxidative stress activates HIF-1α to mediate the secretion of CXCL9 and CXCL10 in keratinocytes and trigger the abnormal immune response in vitiligo.

The oxidative stress regulatory mechanism of autophagy and apoptosis in lens epithelial cells.

The flavonoid GL-V9 induces oxidative stress mediated apoptosis in small cell lung cancer by promoting STEAP3 degradation.

Amlodipine mitigates Cisplatin- and acetaminophen-induced nephrotoxicity associated with alterations in renal gamma-glutamyl transpeptidase and oxidative stress.

A simple, stability-indicating RP-HPLC method was developed to estimate isoliquiritigenin (ISL) and assess its stability under acid, alkaline, oxidative, thermal, and UV stress conditions. Chromatographic separation was performed on a C18 column using UV-visible detection and a 20 μL injection volume, applying an isocratic elution approach to develop and optimize a method for quantifying ISL in stressed samples. At a constant flow rate of 1 mL/min, the mobile phase consisted of 0.1% v/v formic acid (aqueous) and acetonitrile (organic) in a 25:75 ratio. The maximum absorption wavelength (λmax) of ISL was found to be 361 nm. According to ICH Q2(R2) guidelines, the method was validated and showed linearity in the 2-10 μg/mL range (R = 0.9985) with high accuracy (98.38%-99.48% recovery) and precision (% RSD < 2%). Quantification and detection limits were 1.81 and 0.66 μg/mL, respectively. According to forced degradation testing, there was very little deterioration when subjected to thermal and photolytic stress, but there was considerable degradation when exposed to alkaline (93.40%), acidic (98.76%), and oxidative stress (63.80%) at 70°C. The developed method effectively evaluates ISL stability in both bulk and stressed conditions, supporting its use in routine quality control and pharmaceutical formulation.

Retinal pigment epithelial (RPE) cells are particularly vulnerable to oxidative stress. Neighboring choroidal melanocytes (CMs) secrete trophic factors, such as pigment epithelium-derived factor (PEDF) and osteopontin (OPN), which may mitigate oxidative damage in RPE cells. Herein, we investigated the ability of PEDF and OPN to protect RPE cells from extended NaIO3-induced oxidative stress damage. Primary human RPE cells were seeded on plastic (2D culture) or on a 3D tissue-engineered choroidal stroma (TECS) containing (or not) CMs. PEDF or OPN was added before, during, and after 5 days of NaIO3 exposure. Analyses included assessment of PEDF and OPN expression, intracellular reactive oxygen species (ROS), lipid peroxidation, mitochondrial superoxide, cell death, antioxidant capacity (TAC) and p-Nrf2 nuclear translocation. Adding exogenous PEDF to the growth media stimulated de novo PEDF secretion by RPE cells, whereas OPN concentration detected in the growth media corresponded to the amount added. PEDF and OPN levels were consistently lower in the growth media of 3D TECS compared to the 2D cultures. Oxidative stress significantly increased intracellular ROS, lipid peroxidation, and RPE cell death in both 2D and 3D cultures, which were reduced by PEDF or OPN supplementation. Oxidative stress and PEDF or OPN supplementation did not alter the TAC of RPE cells. PEDF or OPN supplementation promoted p-Nrf2 nuclear translocation in RPE cells on plastic, even without oxidative stress, whereas this response was not observed in 3D TECS cultures. Adding CMs to the 3D TECS did not influence p-Nrf2 nuclear translocation in RPE cells. Overall, PEDF and OPN supplementation significantly protected human RPE cells against NaIO3-induced oxidative stress damage. In 3D TECS, CMs secreted insufficient levels of PEDF and OPN for RPE cells to manage oxidative stress-induced damage. These findings demonstrate that exogenous supplementation with PEDF and OPN proteins may be beneficial for oxidative-stress related eye diseases.

Drug-induced liver injury (DILI) from acetaminophen (APAP) overdose involves ER stress, oxidative damage, apoptosis, and inflammation. This study assesses Terminalia arjuna bark extract (TAE) against APAP-induced toxicity in rats, comparing its efficacy with N-acetylcysteine (NAC) through key signaling and inflammatory markers. Twenty-four Wistar rats were equally divided into four groups: Control Negative (CN, no treatment), Control Positive (CP, acetaminophen 350 mg/kg), N-acetylcysteine (NAC, 150 mg/kg), and Terminalia arjuna bark extract (TAE, ethanolic, 80 mg/kg). Over 14 days, liver injury was induced in the CP group via acetaminophen, while the NAC and TAE groups received their respective treatments. Animals were decapitated on day 15, and biological samples were collected for analysis. Biochemical assessments included liver function markers (ALT, AST) and oxidative stress parameters (SOD, TAC, TBARS, TOS). Gene expression studies were performed for oxidative stress regulators (Keap1, Nrf2) and ER stress signaling molecules (ERK, JNK, PPAR-α, AKT). Histopathological examination evaluated liver architecture and cellular integrity. Acetaminophen induced significant hepatotoxicity, as reflected by elevated liver enzymes, increased oxidative stress, altered gene expression, and disrupted liver histology. APAP toxicity resulted in elevated oxidative stress, apoptosis, inflammation, and ER stress, leading to significant hepatic damage (p < 0.0001 vs CN). NAC and TAE treatments mitigated these effects, with TAE demonstrating superior improvement in oxidative stress markers (p < 0.0001 vs CP). Gene expression analysis revealed a protective shift in the Keap1-Nrf2 pathways in the treated groups. Histopathology confirmed reduced necrosis and preserved hepatic architecture in the NAC and TAE groups. T. arjuna exhibits potent hepatoprotective effects, comparable to NAC, through modulation of oxidative stress, apoptosis, and ER stress pathways. Further studies are needed to explore its clinical applicability in acute liver injury management.

Hyperoside as a promising multi-target candidate for neovascular age-related macular degeneration. mechanisms involving Wnt/β-catenin signaling, oxidative stress, and inflammation suppression.