Antioxidants最新文献

{"title":"Nanoantioxidants: Structure-Activity Relationships, Redox Mechanisms, Applications, and Safety.","authors":"Min Ook Kim","doi":"10.3390/antiox15091177","DOIUrl":"10.3390/antiox15091177","url":null,"abstract":"<p><p>Oxidative stress contributes to disease progression, food deterioration, agricultural losses, and material degradation, whereas many conventional antioxidants are limited by poor stability, low bioavailability, rapid consumption, or inadequate delivery. In this review, nanoantioxidants are defined as nanoscale systems intentionally designed to suppress or regulate damaging oxidative processes, and four functional categories are distinguished: intrinsically antioxidant nanomaterials, antioxidant nanozymes, antioxidant-functionalized nanoparticles, and nanocarriers used to deliver conventional antioxidants. The review systematically examines how particle size and surface area, morphology and exposed facets, oxidation state and defect density, surface chemistry and charge, aggregation, dissolution or ion release, dose, and the surrounding environment determine antioxidant activity. Particular emphasis is placed on the context-dependent transition from antioxidant to pro-oxidant behavior, the distinction between enzyme-like nanozyme activity and true enzymatic activity, and the need for nanoparticle-specific controls and complementary assays to avoid analytical interference. Evidence from chemical assays, cell culture, animal studies, and clinical research is considered separately because activity in a simplified chemical system does not by itself establish therapeutic efficacy or safety. Applications in nanomedicine, food preservation, agriculture, environmental protection, and engineering materials are critically compared. Long-term toxicity, biodistribution, clearance, degradation, environmental fate, and life-cycle impacts are highlighted as essential translational criteria; likewise, green synthesis is not treated as synonymous with sustainability without consideration of energy, solvents, purification, scalability, waste, and end-of-life behavior. Future progress will require standardized datasets and experimental protocols, mechanism-guided design, realistic validation, and carefully governed artificial-intelligence-assisted optimization.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057295","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":"Agri-Food Wastes as Natural Source of Bioactive Antioxidants: Fourth Edition.","authors":"Silvana Hrelia, Maria Cristina Barbalace, Cristina Angeloni","doi":"10.3390/antiox15091175","DOIUrl":"10.3390/antiox15091175","url":null,"abstract":"<p><p>The increasing production of agri-food waste represents one of the major challenges to the sustainability of modern food systems [...].</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057001","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":"Oxidized-Lipid Signaling and Ferroptosis as Downstream Mechanisms of Titanium-Associated Peri-Implant Bone Loss.","authors":"Łukasz Woźniak, Bożena Antonowicz, Żaneta Anna Mierzejewska, Ewelina Kosicka, Jérôme R Lechien, Luigi Angelo Vaira, Jan Borys","doi":"10.3390/antiox15091174","DOIUrl":"10.3390/antiox15091174","url":null,"abstract":"<p><p>Titanium and its alloys remain the dominant materials in oral implantology, but degradation products released through corrosion, tribocorrosion, and wear are biologically active. This critical narrative review examines oxidized-lipid signaling and ferroptosis as candidate downstream mechanisms connecting titanium-associated redox dysregulation with peri-implant bone loss. A targeted literature search of PubMed, Web of Science, and Scopus was updated through 2 August 2026 and integrated evidence from dental peri-implant studies, titanium-particle osteolysis models, and broader skeletal research. Titanium-derived particles can promote mitochondrial and non-mitochondrial reactive oxygen species, membrane phospholipid peroxidation, reactive aldehyde formation, and oxidized-phospholipid signaling. Experimental titanium-particle models demonstrate GPX4 repression and osteoblast ferroptosis, while skeletal studies indicate that ferroptotic dysfunction of osteoblasts and osteocytes can impair mineralization, increase the RANKL/OPG ratio, and favor osteoclastogenesis. Human peri-implant fluid data provide emerging but non-diagnostic evidence, including altered GPX4 and malondialdehyde levels. Specialized pro-resolving mediators may counterbalance the destructive lipid-peroxidation branch. Current evidence supports a biologically plausible and experimentally testable pathway rather than established causation in human dental peri-implant tissues. Direct tissue-level confirmation using redox lipidomics, iron mapping, pathway-specific rescue experiments, and spatial osteoimmune profiling is required.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057169","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":"Guanidinoacetic Acid and Cysteamine Hydrochloride Improve Beef Cattle Growth and Antioxidant Capacity via Fecal Microbiome and Serum Metabolome.","authors":"Baoshan Feng, Hongwei Zhang, Jianjun Guo, Meishu Tan, Sen Mao, Bin Yu, Yiran Xu, Yanan Wang, Man Feng, Lianjie Song, Yinghao Zhou, Hongjian Xu","doi":"10.3390/antiox15091178","DOIUrl":"10.3390/antiox15091178","url":null,"abstract":"<p><p>Balancing muscle growth and antioxidant/anti-inflammatory homeostasis is a core requirement for modern beef production. This study investigated whether cysteamine hydrochloride (CSH) co-supplementation with guanidinoacetic acid (GAA) enhances growth and antioxidant status through fecal microbiome and serum metabolome modulation in Simmental beef cattle. A 60-day trial randomly assigned 45 10-month-old cattle to control (CON), GAA-supplemented, and GAA + CSH-supplemented groups (<i>n</i> = 15 per group). Growth performance was recorded throughout the trial. Fecal samples were collected for 16S rRNA sequencing, and serum samples for non-targeted metabolomics. Both GAA and GAA + CSH (GCSH) improved growth performance versus CON (<i>p</i> < 0.05), with no differences between supplemented groups. However, GCSH uniquely elevated antioxidant enzymes and reduced malondialdehyde (<i>p</i> < 0.05). GCSH treatment was associated with higher abundance of <i>Adlercreutzia</i>, <i>Anaerofustis</i>, and <i>Monoglobus</i>, alongside elevated indole-3-propionic acid and salicylsulfuric acid. In contrast, GAA reduced phenylacetyl-L-glutamine and indole-3-acetic acid. iCAMP analysis revealed that GCSH relieved homogenizing selection while enhancing heterogeneous selection, promoting beneficial taxa colonization. GAA primarily enhances nitrogen utilization, while CSH enriches beneficial microbiota and antioxidant metabolites. These findings suggest that GAA and CSH co-supplementation improves growth and antioxidant homeostasis through complementary mechanisms.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057252","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":"Circulating Endothelial Nitric Oxide Synthase on the First Postpartum Day: An Exploratory Cross-Sectional Study of Its Association with Maternal Age, Redox-Relevant Haematological and Lipid Markers, and Postnatal Depression Screening.","authors":"Cristina Dragomir, Mihai Mitulețu, Ioana Muntean, Călin Muntean, Peter Seropian, Ionuț-Marcel Cobec, Roxana Popescu","doi":"10.3390/antiox15091176","DOIUrl":"10.3390/antiox15091176","url":null,"abstract":"<p><p>(1) Background: Endothelial nitric oxide synthase (eNOS/NOS3), the main source of vascular nitric oxide (NO), generates superoxide instead of NO when oxidative stress uncouples it. Circulating eNOS in the early puerperium is uncharacterised. (2) Methods:In a single-centre cross-sectional study (Timișoara, Romania, July 2022), 40 mother-newborn dyads were evaluated. Maternal serum eNOS protein was quantified by ELISA on postpartum day 1, alongside pre-delivery laboratory data and Edinburgh Postnatal Depression Scale (EPDS) screening. Analyses (Spearman correlation, linear regression, prevalence odds) were unadjusted for multiplicity; only correlations of |ρ| ≥ 0.44 were detectable at 80% power. (3) Results:Median serum eNOS was 8.997 ng/mL (interquartile range 4.091-27.985). eNOS correlated inversely with total and LDL cholesterol (ρ = -0.368, <i>p</i> = 0.027; ρ = -0.412, <i>p</i> = 0.013) and positively with erythrocyte count (ρ = 0.326, <i>p</i> = 0.046). The association with maternal age was similar in magnitude but non-significant (ρ = -0.303, <i>p</i> = 0.061). Multivariable models were not significant, and eNOS was unrelated to EPDS score (ρ = 0.111, <i>p</i> = 0.512). (4) Conclusions:Lower circulating eNOS protein, not enzyme activity, accompanied a less favourable lipid profile, but not depressive symptoms. These single-centre Romanian findings are hypothesis-generating and should not be generalised.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057223","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":"A Higher Burden of Abnormal Antioxidant-, Nutritional-, and Inflammation-Related Biomarkers Is Associated with Shoulder-Hand Syndrome, Hand Edema, and Short-Term Upper-Limb Outcomes During Stroke Rehabilitation.","authors":"Ki-Hyeok Ku, Eo Jin Park","doi":"10.3390/antiox15091173","DOIUrl":"10.3390/antiox15091173","url":null,"abstract":"<p><p>Post-stroke shoulder-hand syndrome and hand edema can complicate inpatient rehabilitation and may reflect interactions between antioxidant, nutritional, inflammatory, and neuro-musculoskeletal factors. This single-center retrospective cohort study included 453 adults admitted for inpatient rehabilitation within 60 days after a first-ever unilateral ischemic or hemorrhagic stroke between 1 January 2018 and 31 December 2025. The primary exposure was the number of abnormal antioxidant-, nutritional-, and inflammation-related biomarkers, defined as serum zinc <70 µg/dL, albumin <3.5 g/dL, C-reactive protein ≥1.0 mg/dL, and neutrophil-to-lymphocyte ratio ≥3.0. The primary outcome was shoulder-hand syndrome or clinically significant hand edema during inpatient rehabilitation. In multivariable logistic regression with robust standard errors, each 1-unit increase in the number of abnormal biomarkers was associated with higher odds of the primary composite outcome (odds ratio, 1.43; 95% confidence interval, 1.15-1.77; <i>p</i> = 0.001). Directionally consistent associations were observed for shoulder-hand syndrome, clinically significant hand edema, Fugl-Meyer upper-extremity score at discharge, and poor upper-limb function at discharge. In a temporal sensitivity analysis excluding the 28 patients with the primary outcome already documented at PM&R admission (<i>N</i> = 425), biomarker profiling preceded the documented outcome in all 98 subsequent event cases, and the association remained (odds ratio, 1.42; 95% confidence interval, 1.12-1.79; <i>p</i> = 0.004). These findings indicate that a higher burden of abnormal antioxidant-, nutritional-, and inflammation-related biomarkers was associated with a clinical profile characterized by upper-limb complications and less favorable short-term motor function; the burden measure is not validated for prediction.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057021","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":"Supraphysiological Estrogen Induces Endometrial Impairments via Mitochondrial ROS-Driven NLRP3 Inflammasome Activation.","authors":"Yiran Sun, Hao Yang, Lu Lu, Jiangxue Cai, Chenxi Liu, Jianguo Zhu, Bin He","doi":"10.3390/antiox15091170","DOIUrl":"10.3390/antiox15091170","url":null,"abstract":"<p><p>Exogenous gonadotropin-based estrus synchronization is widely used in livestock reproduction. However, this hormonal treatment has been associated with adverse reproductive outcomes, suggesting that it may alter the uterine environment and endometrial receptivity, although the underlying molecular mechanism remains poorly understood. Here, we investigated the endometrial responses to gonadotropin-induced estrus synchronization using both <i>in vivo</i> and <i>in vitro</i> models. We found that gonadotropin treatment caused structural and inflammatory changes in the endometrium of both pigs and mice, accompanied by elevated circulating estradiol (E₂) levels and enhanced NLRP3 inflammasome-related signaling. In mice, gonadotropin treatment also altered the expression of MUC1, Hand2, and HoxA11, indicating disruption of molecular features associated with endometrial receptivity. In porcine endometrial epithelial cells, supraphysiological E₂ exposure induced mitochondrial oxidative stress, characterized by increased mitochondrial reactive oxygen species production, loss of mitochondrial membrane potential, increased cellular mtDNA abundance, and oxidative DNA damage. E₂ treatment further promoted NLRP3 inflammasome-associated signaling and ASC speck formation, whereas antioxidant N-acetyl-L-cysteine treatment attenuated ASC speck formation. Collectively, these findings support a link between high E₂ exposure, mitochondrial oxidative stress, and enhanced NLRP3 inflammasome signaling in endometrial epithelial cells. Our results suggest that an E₂-mitochondrial oxidative stress-NLRP3 axis may contribute to gonadotropin-associated endometrial dysfunction and provide a basis for further investigation of antioxidant and inflammasome-targeted strategies in livestock reproduction.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057357","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":"Antioxidant Interventions on Muscle Function and Mass in Aging-Related Muscle Decline: A Systematic Review of Preclinical and Clinical Evidence.","authors":"Xin Li, Ke Zhou, Ronald Man Yeung Wong, Wing Hoi Cheung, Can Cui","doi":"10.3390/antiox15091167","DOIUrl":"10.3390/antiox15091167","url":null,"abstract":"<p><p>Oxidative stress contributes to aging-related muscle decline, but antioxidant interventions may affect functional and structural outcomes differently. This systematic review synthesized clinical, animal, and cellular evidence across clinically defined sarcopenia and broader models of aging-related muscle decline. PubMed, Embase, Web of Science, and Cochrane Central Register of Controlled Trials (CENTRAL) were searched through 11 July 2026. Eligible studies tested antioxidant interventions in older adults or aging-related preclinical models and were appraised using the Cochrane Risk of Bias 2 (RoB 2) tool, a modified Systematic Review Centre for Laboratory animal Experimentation (SYRCLE) risk-of-bias tool, and a modified in vitro checklist. Forty-four publications were included: eight clinical trials, 26 animal datasets, and 18 cellular datasets, with eight publications contributing both animal and cellular evidence. Comparative clinical benefits were reported primarily for strength or power (7/8 studies), with less support for physical performance (2/6 studies assessing this domain) or body composition-related muscle quantity (2/8 studies). Selected preclinical studies likewise showed functional gains without parallel structural improvement, although effects varied by model and intervention. Preclinical findings implicated antioxidant defense, mitochondrial maintenance, inflammation, and proteostasis, but most pathway evidence was associative and direct experimental validation was limited. Clinical evidence was further constrained by small samples, short interventions, combined nutritional or exercise co-interventions, and heterogeneous outcomes. Current evidence does not support a consistent increase in muscle quantity with antioxidant interventions. The observed pattern appears context dependent and requires confirmation in adequately powered, phenotype-stratified trials assessing muscle strength, physical performance, muscle quantity, and mechanistic endpoints.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056984","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":"Glycerol Monolaurate Supplementation in Extruded Diets Enhances Immune Function and Antioxidant Capacity and Alters the Gut Microbiota and Fecal Metabolome in Cats.","authors":"Haotian Jiang, Bo Liu, Jialin Zhang, Xin Ge, Zhonghui Jin, Shuaijuan Han, Shudong Liu","doi":"10.3390/antiox15091169","DOIUrl":"10.3390/antiox15091169","url":null,"abstract":"<p><p>This study evaluated the effects of dietary glycerol monolaurate (GML) supplementation on feline growth performance and intestinal health. Twenty-four adult British Shorthair cats (3.03 ± 0.07 kg) were initially enrolled. Following a 56-day pre-feeding period, 18 eligible cats were allocated to two dietary groups, of which 12 cats were prespecified for final sample collection and statistical analysis (<i>n</i> = 6): a control group (CON, basal diet) and an experimental group (EXP, basal diet + 2000 mg/kg GML product) for a 28-day trial. Dietary GML significantly increased the average daily feed intake. GML supplementation significantly increased the changes in fecal score and fecal pH, and a significant GML × day interaction was observed for the change in fecal pH. GML improved the apparent digestibility of dry matter, gross energy, crude fat, and crude protein. Furthermore, serum albumin increased within the normal range. Cats in the EXP group showed elevated antioxidant enzyme activities, alongside lower malondialdehyde concentrations. GML also elevated serum immunoglobulin A and reduced pro-inflammatory cytokines. Fecal analyses showed reduced acetic acid and total volatile fatty acids, but elevated propionic acid. Microbiome and metabolomic profiling revealed that GML decreased the relative abundance of <i>Streptococcus</i> and metabolites such as Linoleic Acid and 12,13-Epome, while increasing the relative abundances of <i>Collinsella</i>, <i>Peptoclostridium</i>, <i>Clostridium</i>, and (-)-Jasmonic Acid. These findings provide a theoretical foundation for applying GML in pet foods to optimize companion animal extruded diets.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057261","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":"Resveratrol's Neuroprotective Effects on the Retina in a Pentylenetetrazol-Induced Epilepsy Model in Rats: Insights into SIRT1 Signaling, Apoptosis, and Gliosis.","authors":"Omer Unal, Nilufer Akgun-Unal, Elif Gulbahce-Mutlu, Seda Simsek, Mustafa Ayyildiz","doi":"10.3390/antiox15091168","DOIUrl":"10.3390/antiox15091168","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background/objectives: &lt;/strong&gt;A chronic neurological disorder known as epilepsy results in neurodegeneration, oxidative stress, and damage to the retina and the central nervous system's structure. The main objective of this research was to examine the neuroprotective benefits of Resveratrol (RES) on the retina in a model using Pentylenetetrazol (PTZ) in rats to induce kindling and to investigate the underlying molecular and biochemical mechanisms (SIRT1, GFAP, VEGF, apoptotic pathways, and oxidative stress markers [malondialdehyde (MDA) and reduced glutathione (GSH)] of this protective effect.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A total of thirty-two male Wistar albino rats were randomly assigned to four distinct groups: Sham, RES (5 mg/kg/day), PTZ (35 mg/kg), and PTZ + RES (&lt;i&gt;n&lt;/i&gt; = 8 per group). Electrocorticography (ECoG) recordings were used to assess seizure severity. Retinal expression of GFAP, VEGF, SIRT1, Bax, Bcl-2, Caspase-3, and Caspase-9 was evaluated via qPCR and immunofluorescence, while tissue lipid peroxidation (MDA) and reduced glutathione (GSH) levels were quantified spectrophotometrically to directly evaluate retinal redox status.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Substantial increases in seizure scores and electrocorticogram spike counts were noted in the PTZ group, whereas RES treatment significantly reduced the total ECoG spike count by 49.6% (from 702.87 ± 145.82 in PTZ to 354.25 ± 31.22 in PTZ + RES, &lt;i&gt;p&lt;/i&gt; &lt; 0.0001) and lowered the average seizure stage from 4.25 ± 0.27 to 2.43 ± 0.49 (&lt;i&gt;p&lt;/i&gt; &lt; 0.05), while lengthening the initial myoclonic jerk latency (from 162 ± 29.62 s to 219.37 ± 32.12 s, &lt;i&gt;p&lt;/i&gt; &lt; 0.01). Molecular and histopathological analyses revealed that RES treatment was associated with enhanced localized retinal cell survival and a significant increase in the nuclear SIRT1 immunofluorescence area fraction in the retina, which more than doubled the nuclear SIRT1 immunofluorescence area fraction in the retina (from 4.2 ± 0.9% in PTZ to 8.4 ± 0.8% in PTZ + RES, &lt;i&gt;p&lt;/i&gt; &lt; 0.05) despite a physiological transcription-level feedback reduction in SIRT1 mRNA. Furthermore, RES treatment significantly suppressed PTZ-induced retinal apoptosis (Caspase-3 area fraction decreased from 10.6 ± 0.9% to 5.6 ± 0.8%, &lt;i&gt;p&lt;/i&gt; &lt; 0.001) and attenuated reactive gliosis (GFAP area fraction decreased from 14.1 ± 1.2% to 9.1 ± 1.4%, &lt;i&gt;p&lt;/i&gt; &lt; 0.01). Biochemically, PTZ kindling induced a profound increase in retinal lipid peroxidation (MDA) and a severe depletion of reduced glutathione (GSH) reserves, both of which were robustly reversed by RES treatment back toward physiological Sham levels (&lt;i&gt;p&lt;/i&gt; &lt; 0.01).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Chronic epilepsy causes glial activation, oxidative damage, and apoptosis in the retina, with RES-associated retinal protection involving the restoration of redox homeostasis and the upregulation of the SIRT1 signaling pathway. These preclinical findings suggest that RES represen","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 9","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057208","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}