Antioxidants

Edible Grass (EG) is a hybrid vegetable variety valued for its high biomass and protein content, garnering significant interest in recent years for its potential in food, feed, and health product applications. However, in subtropical climates, intense light and high temperatures severely affect the growth and development of Edible Grass (EG), leading to substantial reductions in yield and quality. This study was conducted in the subtropical humid monsoon climate zone of Changsha, Hunan, China, comparing two growth conditions: natural light (CK) and shading treatment (ST). High light-aggravated heat damage under CK significantly reduced EG yield and quality (p < 0.05), with severe cases leading to plant death. and could even lead to plant death in severe cases. Specifically, maximum air and leaf temperatures under CK reached 38.85 °C and 38.14 °C, respectively, well exceeding the plant’s optimal growth range. Shading treatment (ST) effectively alleviated this damage, significantly increasing the net photosynthetic rate, stomatal conductance, and intercellular CO₂ concentration, while decreasing leaf temperature and transpiration rate (p < 0.001). The analysis of physiological and biochemical indicators indicates that after ST, the activities of SOD, CAT, and POD in the leaves decreased, while the contents of MDA and H₂O₂ were significantly lower compared to the CK group (p < 0.001). The transcriptome sequencing results indicate that a total of 8004 DEGs were identified under shading treatment (ST) relative to natural light (CK), with 3197 genes upregulated and 4807 genes downregulated. Significantly enriched Gene Ontology (GO) terms include ‘cell membrane’, ‘extracellular region’, and ‘protein kinase activity’, while significantly enriched KEGG metabolic pathways include ‘plant hormone signal transduction’, ‘photosynthesis–antenna proteins’, and ‘glutathione metabolism’. Compared to CK, the expression of genes associated with oxidative stress (e.g., CAT1, OXR1, APX, GPX) was significantly downregulated in ST, indicating a relief from light-aggravated heat stress. This transcriptional reprogramming was corroborated by metabolomic data, which showed reduced accumulation of key flavonoid compounds, aligning with the downregulation of their biosynthetic genes as well as genes encoding heat shock proteins (e.g., Hsp40, Hsp70, Hsp90). It indicated that plants switch from a ‘ROS stress–high energy defense’ mode to a ‘low oxidative pressure–resource-saving’ mode. Collectively, ST significantly alleviated the physiological damage of forage grasses under heat stress by modulating the processing of endoplasmic reticulum heat stress proteins, plant hormones, and related genes and metabolic pathways, thereby improving photosynthetic efficiency and yield. The findings provide a theoretical basis for optimizing the cultivation management of EG, particularly in subtropical regions, where shade treatment serves as an effective agronomic strategy to significantly enhance the stress resistance and yield of EG.

Recently, extreme weather has been regarded as a risk factor for exacerbating allergic airway inflammation (AAI), but its underlying mechanism remains unclear. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has been implicated in various lung diseases. This study investigated whether cold exposure aggravated OVA-induced AAI by promoting ferroptosis. A murine AA model was established using OVA sensitization and challenge. Mice were exposed to cold temperatures (10 °C or 4 °C) for 4 h daily. Ferroptosis was assessed by measuring ferroptosis-related markers (GPX4, ACSL4, FTL), iron deposition (Alcian Blue-Periodic Acid-Schiff Staining), lipid peroxidation (MDA), antioxidant levels (GSH), and mitochondrial ultrastructure (TEM). The ferroptosis inhibitor ferrostatin-1 (Fer-1) was administered to evaluate its protective effects. Airway inflammation, lung function, and histopathology were also analyzed. Cold exposure significantly worsened AA symptoms, including increased Th2 cytokine levels (IL-4, IL-5, IL-13, IL-33), impaired lung function, and enhanced airway remodeling and mucus production. These effects were more pronounced at 4 °C. Cold exposure also induced ferroptosis, as evidenced by decreased GPX4 and FTL, increased ACSL4, elevated iron and MDA levels, reduced GSH, and mitochondrial damage. Treatment with Fer-1 mitigated these changes, alleviating inflammation, improving lung function, and reducing histological damage. Cold exposure exacerbated AAI by inducing ferroptosis in lung tissues. Inhibition of ferroptosis with Fer-1 attenuated these aggravation effects, suggesting ferroptosis as a potential mechanistic link between cold exposure and AAI severity. Targeting ferroptosis might offer a novel therapeutic strategy for mitigating AAI under cold conditions.

High-risk neuroblastoma (NB) is an aggressive pediatric tumor characterized by pronounced biological heterogeneity and frequent development of chemoresistance, which critically limits therapeutic efficacy. Identifying novel anti-NB agents remains an urgent unmet need. To address this, we designed and synthesized 17 hybrid molecules by combining natural antioxidant scaffolds (coumarin, vanillin, and isovanillin) through an acyl-hydrazone linker. Several derivatives significantly reduced the viability of MYCN-amplified NB cells (HTLA-230) and their multi-drug resistant counterpart (ER) while not affecting human keratinocytes (HaCat). Among them, compounds 5, 9 and 12 selectively inhibited HTLA and ER growth (10–25%) without affecting HaCat, accompanied by robust ROS overproduction, particularly by 9 and 12 (up to 40%). None of these compounds induced apoptosis or ferroptosis. Instead, their antiproliferative effects were associated with senescence induction and, only for compound 5, with a decrease in clonogenic potential. Moreover, to further characterize compounds 5, 9, and 12, the analysis was extended across other human neuroblastoma cell lines. In parallel, the effects of the compounds on non-malignant cell lines were assessed to obtain an indication of their selectivity toward tumor cells. Compound 17, a structural analog lacking the second aromatic ring in the ex-aldehyde portion, displayed a distinct profile with a limited anticancer activity, underscoring the importance of this structural fragment for antiproliferative efficacy.