Antioxidants最新文献

{"title":"Betulinic Acid-Enriched <i>Dillenia indica</i> L. Bark Extract Attenuates UVB-Induced Skin Aging via KEAP1-Mediated Antioxidant Pathways.","authors":"Bo-Rim Song, Sunghwan Kim, Sang-Han Lee","doi":"10.3390/antiox14091144","DOIUrl":"10.3390/antiox14091144","url":null,"abstract":"<p><p>The bark of <i>Dillenia indica</i> L. is a rich source of phenolic and triterpenoid compounds, including betulinic acid (BA), known for their antioxidant and anti-aging properties. This study investigated the antioxidant potential of a BA-enriched extract through a multidisciplinary approach combining computational, experimental, and cell-based evaluations. Molecular docking and molecular dynamics simulations revealed that BA binds stably to Kelch-like ECH-associated protein 1 (KEAP1), suggesting activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Extraction conditions were optimized using response surface methodology (RSM) and artificial neural network (ANN) modeling, yielding the maximum total phenolic content (TPC; 85.33 ± 2.26 mg gallic acid equivalents/g) and total flavonoid content (TFC; 75.60 ± 1.66 mg catechin equivalents/g), with ANN demonstrating superior predictive performance compared to RSM. Electrospray ionization tandem mass spectrometry (ESI-MS/MS) confirmed the presence of BA in the optimized extract. Simulated gastrointestinal digestion revealed reductions in TPC, TFC, and radical scavenging activity during the gastric phase. In ultraviolet B (UVB)-irradiated human keratinocyte (HaCaT) cells, the optimized extract significantly reduced intracellular reactive oxygen species (ROS) and upregulated the KEAP1-Nrf2-heme oxygenase-1 (HO-1) pathway, confirming its antioxidant mechanism. These findings highlight the extract's stability, bioactivity, and mechanistic efficacy, supporting its application as a nutraceutical ingredient for combating oxidative stress and skin aging.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sheng Mai San Mitigates Heat Stress-Induced Myocardial Injury by Coordinated Regulation of the Keap1-Nrf2-HO-1 and Stub1-HSF1 Signaling Pathways.","authors":"Jiaqi Dong, Qian Ma, Rong Yang, Xiaosong Zhang, Yongli Hua, Peng Ji, Wanling Yao, Ziwen Yuan, Yanming Wei","doi":"10.3390/antiox14091140","DOIUrl":"10.3390/antiox14091140","url":null,"abstract":"<p><p>Heat stress (HS), a pervasive environmental stressor, significantly disrupts systemic physiological homeostasis, posing substantial threats to human and animal health. Sheng Mai San (SMS), a classic Traditional Chinese Medicine (TCM) formula, exerts its therapeutic effects by replenishing qi (the vital energy governing physiological functions) and nourishing yin (the material basis responsible for moistening and cooling actions). This formula demonstrates significant efficacy in astringing sweating and preventing collapse. However, its precise molecular mechanisms against HS-induced myocardial injury remain incompletely elucidated. This study initially employed physicochemical analytical methods to determine the contents of total polysaccharides, saponins, and flavonoids in SMS and evaluated its antioxidant activity. Subsequently, both in vitro and in vivo rat models of HS were established to systematically assess the alterations in reactive oxygen species (ROS), antioxidant enzymes (GSH, SOD, CAT), and heat shock proteins (HSP70, HSP90) following SMS intervention, thereby investigating HS-induced myocardial injury and the protective effects of SMS. Furthermore, Western blot, immunofluorescence, and qRT-PCR techniques were utilized to quantitatively analyze key molecules in the Keap1-Nrf2-HO-1 and Stub1-HSF1 signaling pathways. The results demonstrated that total polysaccharides were the most concentrated in SMS, followed by total saponins. This formula exhibited potent free radical scavenging capacity against DPPH, ABTS, and OH^-, along with significant reducing activity. HS-induced myocardial injury reached its peak severity at 6-12 h post-stress exposure. SMS intervention effectively suppressed excessive ROS generation, enhanced the activities of antioxidant enzymes (GSH, SOD, and CAT), and downregulated HSP70 and HSP90 mRNA expression levels, thereby significantly mitigating cardiomyocyte damage. Mechanistic investigations revealed that SMS conferred cardioprotection through dual modulation of the Keap1-Nrf2-HO-1 and Stub1-HSF1 signaling pathways. This study not only provides a novel TCM-based therapeutic strategy for preventing and treating HS-related cardiovascular disorders but also establishes a crucial theoretical foundation for further exploration of SMS's pharmacological mechanisms and clinical applications.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of Pulmonary Inflammation and the Redox Pathway In Vitro and In Vivo by Fumaric Ester.","authors":"Aline Pontes de Oliveira, Alexsandro Tavares Figueiredo-Junior, Priscilla Cristine de Oliveira Mineiro, Evelyn Caribé Mota, Carolinne Souza de Amorim, Helber da Maia Valenca, Aline Cristina Casimiro de Albuquerque Gomes, Sabrina Sodré de Souza Serra, Pedro Leme Silva, Christina Maeda Takiya, João Alfredo de Moraes, Samuel Santos Valenca, Manuella Lanzetti","doi":"10.3390/antiox14091141","DOIUrl":"10.3390/antiox14091141","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is characterized by chronic pulmonary inflammation and the destruction of the pulmonary parenchyma (emphysema), with only symptomatic treatment available. Molecules with antioxidant and anti-inflammatory properties, such as dimethyl fumarate (DMF), have shown therapeutic potential. This study evaluated the effects of DMF and its metabolite, monomethyl fumarate (MMF), on pulmonary inflammation induced by cigarette smoke (in vitro) and porcine pancreatic elastase (PPE) in mice (in vivo). In vitro, human pulmonary epithelial cells (PC-9) were treated with MMF at concentrations of 10, 30, and 100 µM and exposed to cigarette smoke extract (CSE) to assess cell viability, oxidative stress (ROS), lipid peroxidation, and nitrite production. In vivo, C57BL/6 mice were treated with DMF (30 and 100 mg/kg) during and after the induction of emphysema by PPE. ROS levels, total cell count in bronchoalveolar lavage fluid (BALF), lung histology, and the expression of oxidative stress proteins (SOD1 and HO-1) were analyzed. MMF reduced oxidative stress and lipid peroxidation under in vitro conditions. In vivo, DMF reduced ROS levels, inflammation, and prevented lung damage, such as alveolar enlargement. The expression of SOD1 and HO-1 was modulated by DMF treatment. The results suggest that DMF could be an effective therapeutic alternative for COPD, reducing oxidative stress and inflammation.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Antioxidants: How Redox Pathways Shape Cellular Signaling and Disease Outcomes.","authors":"Abdallah Alhaj Sulaiman, Vladimir L Katanaev","doi":"10.3390/antiox14091142","DOIUrl":"10.3390/antiox14091142","url":null,"abstract":"<p><p>Cellular redox pathways are critical regulators of various biological processes, including the intricate modulation of intracellular signaling pathways. This review explores how major redox enzymes-such as catalase, superoxide dismutases, glutathione peroxidases, thioredoxins, and peroxiredoxins-interact with key cellular signaling pathways, including receptor tyrosine kinase, mTORC1/AMPK, Wnt/β-catenin, TGF-β/SMAD, NF-κB, Hedgehog, Notch, and GPCR signaling. By investigating mechanisms such as ROS-mediated activation, cysteine oxidation, spatial enzyme localization, and phosphatase regulation, we demonstrate the extensive influence of redox balance on cellular signaling dynamics. Understanding these redox-dependent interactions provides insights into pathophysiological conditions ranging from cancer to fibrosis, offering novel therapeutic opportunities.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulated Expression of Canonical and Non-Canonical Glycolytic Enzyme Isoforms in Peripheral Blood from Subjects with Alcohol Use Disorder and from Individuals with Acute Alcohol Consumption.","authors":"Maura Rojas-Pirela, Daniel Salete-Granado, Diego Andrade-Alviárez, Alejandro Prieto-Rojas, Cristina Rodríguez, María-Lourdes Aguilar-Sánchez, David Puertas-Miranda, María-Ángeles Pérez-Nieto, Vanessa Rueda-Cala, Candy Pérez, Wilfredo Quiñones, Paul A M Michels, Ángeles Almeida, Miguel Marcos","doi":"10.3390/antiox14091143","DOIUrl":"10.3390/antiox14091143","url":null,"abstract":"<p><p>Glycolysis is primarily involved in ATP production but also modulates oxidative stress. Chronic alcohol consumption is correlated with an increased incidence of multiple diseases, including cancer and neurodegenerative diseases (NDDs), though the underlying mechanisms remain unclear. Guided by a literature review and bioinformatics analysis, we evaluated the expression of 22 genes encoding various isoforms of seven glycolytic enzymes (GEs) in the peripheral blood of patients with alcohol use disorder (AUD), individuals with acute alcohol consumption (AAC), and their respective control groups using qPCR. In parallel, we evaluated the expression of selected genes coding for GEs linked to NDDs, as well as astrocytic markers in primary mouse astrocyte cultures exposed to ethanol. Thirteen GE-related genes, including non-canonical isoforms, were significantly dysregulated in AUD patients; notably, eight of these genes showed similar alterations in individuals with AAC. Several enzymes encoded by these genes are known to be regulated by oxidative stress. Ethanol-exposed astrocytes also showed altered expression of glycolytic genes associated with NDDs and astrocyte function. These findings indicate that glycolytic dysregulation is driven by ethanol intake, regardless of exposure duration or organic damage, highlighting a link between ethanol-driven redox imbalance and glycolytic remodeling, which could contribute to organ damage.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.","authors":"Mi Xiang, Mengling Yang, Lijuan Zhang, Xiaohu Ouyang, Alexey Sarapultsev, Shanshan Luo, Desheng Hu","doi":"10.3390/antiox14091138","DOIUrl":"10.3390/antiox14091138","url":null,"abstract":"<p><p>Cardiovascular diseases hinge on a vicious, self-amplifying cycle in which mitochondrial deoxyribonucleic acid (mtDNA) dysfunction undermines cardiac bioenergetics and unleashes sterile inflammation. The heart's reliance on oxidative phosphorylation (OXPHOS) makes it exquisitely sensitive to mtDNA insults-mutations, oxidative lesions, copy-number shifts, or aberrant methylation-that impair ATP production, elevate reactive oxygen species (ROS), and further damage the mitochondrial genome. Damaged mtDNA fragments then escape into the cytosol, where they aberrantly engage cGAS-STING, TLR9, and NLRP3 pathways, driving cytokine storms, pyroptosis, and tissue injury. We propose that this cycle represents an almost unifying pathogenic mechanism in a spectrum of mtDNA-driven cardiovascular disorders. In this review, we aim to synthesize the pathophysiological roles of mtDNA in this cycle and its implications for cardiovascular diseases. Furthermore, we seek to evaluate preclinical and clinical strategies aimed at interrupting this cycle-bolstering mtDNA repair and copy-number maintenance, reversing pathogenic methylation, and blocking mtDNA-triggered innate immune activation-and discuss critical gaps that must be bridged to translate these approaches into precision mitochondrial genome medicine for cardiovascular disease.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomedical Applications of Humic Substances: From Natural Biopolymers to Therapeutic Agents.","authors":"Yana Gvozdeva, Petya Peneva, Plamen Katsarov","doi":"10.3390/antiox14091139","DOIUrl":"10.3390/antiox14091139","url":null,"abstract":"<p><p>Humic substances, which include humic acid and fulvic acid, are natural biopolymers formed from the decomposition of organic matter. There is growing interest in them because of their diverse potential in the biomedical field. Their complex structures, rich in various functional groups, provide antioxidant, anti-inflammatory, antimicrobial, antiviral, and immunomodulatory properties. Recent studies demonstrate that humic substances can scavenge reactive oxygen species, modulate cytokine production, inhibit viral fusion, promote wound healing, and enhance gut microbiota balance. Humic acid and fulvic acid also exhibit anticancer activity by inducing apoptosis in tumor cells, while protecting healthy tissues from oxidative stress. Furthermore, their chelating capacity underlies detoxifying activity and heavy metal binding effects. Despite promising research, variability in composition and potential cytotoxicity under certain conditions emphasize the need for standardized extraction methods and rigorous preclinical evaluation. This review offers a comprehensive overview of the biological effects of humic substances, exploring the mechanisms behind their actions and their potential biomedical applications. It highlights both the benefits and the limitations associated with their use in drug delivery systems.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does the Maternal Gut Microbiome Influence the Outcome of Perinatal Asphyxia?","authors":"Vlad-Petru Morozan, Mara I Ionescu, Carmen M D Zahiu, Ana Maria Catrina, Andreea Racoviță, Ana-Teodora Chirilă, Ioana-Alexandra Dogaru, Cristian Ciotei, Gratiela Gradisteanu Pircalabioru, Ana-Maria Zăgrean","doi":"10.3390/antiox14091134","DOIUrl":"10.3390/antiox14091134","url":null,"abstract":"<p><p>This review explores the maternal gut microbiome's role in shaping neonatal neurodevelopmental outcomes following perinatal asphyxia (PA), a leading cause of infant mortality and disability with limited therapeutic options beyond hypothermia. We synthesized current evidence on microbiome-mediated neuroprotective mechanisms against hypoxic-ischemic brain injury. The maternal microbiome influences fetal development through bioactive metabolites (short-chain fatty acids, indole derivatives) that cross the placental barrier, bacterial antigen regulation, and infant microbiome colonization. These pathways activate multiple protective mechanisms: anti-inflammatory signaling via NF-κB suppression and regulatory T cell expansion; antioxidant defenses through Nrf2 activation; neural repair via BDNF upregulation and neurogenesis; and oxytocin system modulation. Animal models demonstrate that maternal dysbiosis from high-fat diet or antibiotics exacerbates PA-induced brain damage, increasing inflammatory markers and hippocampal injury. Conversely, probiotic supplementation, dietary fiber, and specific interventions (omega-3, resveratrol) reduce neuroinflammation and oxidative injury. Human studies link maternal dysbiosis-associated conditions (obesity, gestational diabetes) with adverse pregnancy outcomes, though direct clinical evidence for PA severity remains limited. Understanding the maternal microbiome-fetal brain axis opens therapeutic avenues, including prenatal probiotics, dietary modifications, and targeted metabolite supplementation to prevent or mitigate PA-related neurological sequelae, potentially complementing existing neuroprotective strategies.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex- and Ethnic-Specific Associations of Serum Lipids with Risk of 12 Cancers: Findings from 506,381 Adults in Two Large Cohorts.","authors":"Minh Nguyen Thien, Ji Woo Baek, Yeun Soo Yang, Sun Ha Jee","doi":"10.3390/antiox14091135","DOIUrl":"10.3390/antiox14091135","url":null,"abstract":"<p><p>The contribution of serum lipids to carcinogenesis, including their effects on inflammation and oxidative stress, remains debated due to inconsistent evidence across populations. This study aimed to elucidate sex- and ethnic-specific associations between serum lipid indices and the risk of 12 common cancers in two large, distinct populations. We conducted a pooled analysis of 506,381 participants from the UK Biobank (UKB) and the Korean Cancer Prevention Study-II (KCPS-II) cohort, with median follow-ups of 12.0 and 13.0 years, respectively. Multivariable-adjusted Cox hazards models were used to estimate hazard ratios (HRs) for the association between baseline lipids and cancer incidence. In the UKB, a one-standard deviation (1-SD) increase in HDL-C was associated with a decreased overall cancer risk (HR 0.982, 95% CI: 0.969-0.995); meanwhile, a 1-SD increase in LDL-C was associated with an increased risk (HR 1.021, 1.009-1.034); higher HDL-C was linked to an increased risk of cervical cancer (HR 1.167, 1.019-1.337) and prostate cancer (HR 1.025, 1.001-1.049). These associations were not significant in the KCPS-II. The association between serum lipids and cancer risk is substantially modified by sex and ethnicity, suggesting that universal lipid-based prevention strategies may be inappropriate and underscoring the need for population-specific research.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinoprotective Effects of Abscisic Acid in Ischemic Retinopathy Mouse Model.","authors":"Inez Bosnyak, Agnes Nagy, Dorottya Molitor, Balazs Meresz, Edina Szabo, Dora Reglodi, Tamas Atlasz, Alexandra Vaczy","doi":"10.3390/antiox14091133","DOIUrl":"10.3390/antiox14091133","url":null,"abstract":"<p><p>The prevalence of hypoxia-caused eye diseases is increasing, but effective, non-invasive treatment options are not available. Abscisic acid (ABA) is a plant hormone with anti-inflammatory and antioxidant effects. ABA is also present in various mammalian tissues and plays an important role in metabolic processes. Therefore, we aimed to investigate the potential protective role of ABA eye drops in ischemic retinopathy. Retinal ischemia was induced by permanent unilateral common carotid artery occlusion (UCCAO) in mice. Half of the animals received ABA eye drops two times a day for two weeks. Optical coherence tomography (OCT) was used to follow the changes in retinal thickness. Moreover, immunohistochemistry and molecular biology methods were used to explore the morphological changes and the underlying mechanisms, respectively. Based on OCT measurements, ischemic retinopathy was successfully developed. The decrease in the thickness of numerous retinal layers could be prevented with ABA eye drops. The ganglion cell number decreased significantly after UCCAO in the central and peripheral regions of the retina. ABA treatment could moderate the damage in both regions. Furthermore, our apoptosis array results suggest that ABA regulates the apoptotic pathways under hypoxic conditions. In conclusion, ABA eye drops may represent a new potential therapeutic option for the treatment of ischemic retinopathy.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}