Antioxidants最新文献

{"title":"The DJ-1-Binding Compound Exerts a Protective Effect in Both In Vitro and In Vivo Models of Sepsis-Induced Acute Kidney Injury.","authors":"Réka Zrufkó, Csenge Pajtók, Beáta Szebeni, Apor Veres-Székely, Mária Bernáth, Csenge Szász, Péter Bokrossy, Attila J Szabó, Ádám Vannay, Domonkos Pap","doi":"10.3390/antiox14060719","DOIUrl":"10.3390/antiox14060719","url":null,"abstract":"<p><p>Although sepsis-induced acute kidney injury (AKI) is associated with significant morbidity and mortality, its treatment remains unresolved. Oxidative stress and inflammation are key elements in the pathomechanism of AKI. Therefore, in the present study, we investigated the role of DJ-1 protein, known for its antioxidant and anti-inflammatory properties in an animal model of lipopolysaccharide (LPS)-induced AKI. The presence of DJ-1 was detected by immunofluorescence staining in mice kidney samples, human embryonic kidney cells (HEK-293), and peripheral blood mononuclear cells (PBMCs). To investigate DJ-1 functions, Compound-23, a specific DJ-1-binding and preserving compound (CAS: 724737-74-0), was used in vitro and in vivo. Compound-23 reduced the H₂O₂-induced reactive oxygen species (ROS) production of the HEK-293 cells, and their LPS- or H₂O₂-induced death, as well. In accordance, Compound-23 decreased the mRNA expression of the oxidative stress markers NAD(P)H quinone dehydrogenase 1 (<i>NQO1</i>) and glutamate-cysteine ligase (<i>GCLC</i>) in the LPS-treated, and <i>NQO1</i> in the H₂O₂-treated cells. Moreover, Compound-23 reduced the H₂O₂- and LPS-induced mRNA expression of inflammatory cytokine interleukin 6 (<i>IL6</i>) in both HEK-293 and PBMCs. Using the mice model of LPS-induced AKI, we demonstrated that Compound-23 treatment improved the renal functions of the mice. In addition, Compound-23 decreased the renal mRNA expression of kidney injury molecule 1 (<i>Kim1</i>), neutrophil gelatinase-associated lipocalin (<i>Ngal</i>), <i>Nqo1</i>, <i>Gclc</i>, and <i>Il6</i> in the LPS-treated mice. Our study revealed that compounds protecting DJ-1 functions may protect the kidney from LPS-induced damage, suggesting that DJ-1 could be a potential drug target for sepsis-induced AKI therapy.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493706","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":"Impact of Diquat on the Intestinal Health and the Composition and Function of the Gut Microbiome.","authors":"Jiao He, Qing Tang, Yan-Cun Liu, Li-Jun Wang, Yan-Fen Chai","doi":"10.3390/antiox14060721","DOIUrl":"10.3390/antiox14060721","url":null,"abstract":"<p><p>Diquat (DQ) is extensively utilized as a herbicide in farming, and its intake can result in serious systemic toxicity due to its induction of oxidative stress (OS) and disruption of intestinal homeostasis. The gastrointestinal tract is one of the first systems exposed to DQ, and damage to this system can influence the general health of the host. Our review summarizes the toxic effects of DQ on the intestinal barrier integrity, gut microbiome, and microbial metabolites (e.g., short-chain fatty acids [SCFAs], bile acids). By elucidating the mechanisms linking DQ-induced OS to gut dysbiosis, mitochondrial dysfunction, and inflammation, our work provides critical insights into novel therapeutic strategies, including probiotics, antioxidants (e.g., hydroxytyrosol, curcumin), and selenium nanoparticles. These findings address a pressing gap in understanding environmental toxin-related gut pathology and offer potential interventions to mitigate systemic oxidative damage.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493714","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":"Scutellarin Alleviates Cuprizone-Induced Demyelination by Improving Mitochondrial Dysfunction, Reducing Lipid Oxidation and Inhibiting the p38 MAPK Pathway.","authors":"Qiting Zhao, Yantuanjin Ma, Shufen Wang","doi":"10.3390/antiox14060723","DOIUrl":"10.3390/antiox14060723","url":null,"abstract":"<p><p>The occurrence of demyelination in the central nervous system (CNS) causes neurodegenerative lesions. The occurrence and development of demyelination involve multiple pathological mechanisms, including the generation of reactive oxygen species (ROS) caused by mitochondrial dysfunction in microglia and subsequent neuroinflammation. Scutellarin is a natural flavonoid drug with significant neuroprotective effects, including antioxidant, anti-inflammatory, and anti-apoptotic properties, and is widely used in the treatment of neurological diseases. However, the protective effects and mechanisms of scutellarin on demyelination have not yet been elucidated. This study aims to investigate the neuroprotective effects of scutellarin on demyelination and its underlying molecular mechanisms. Our results showed that treatment with scutellarin significantly alleviated Cuprizone-induced myelin damage, neuronal apoptosis, and neurological deficits in mice. In in vitro experiments, scutellarin significantly reduced Cuprizone-copper-induced pro-inflammatory microglia formation and inhibited the secretion of TNF-α, thereby reducing myelin cell damage. Mechanism studies revealed that scutellarin inhibited the secretion of TNF-α by microglia and alleviated myelin cell damage by reducing the excessive production of mitochondrial reactive oxygen species (Mito-ROS), reactive oxygen species (ROS), and malondialdehyde (MDA) induced by Cuprizone-copper in microglia. Finally, scutellarin improved mitochondrial dysfunction in microglia and significantly alleviated myelin cell damage by inhibiting the expression of p38MAPK. In conclusion, our findings demonstrate that scutellarin exerts significant neuroprotective effects on Cuprizone-induced mice by improving mitochondrial dysfunction in microglia, thereby reducing inflammatory responses. This effect is closely associated with the inhibition of the p38MAPK pathway.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493775","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":"In Vivo Evidence of Melatonin's Protective Role in Alkylating-Agent-Induced Pulmonary Toxicity: A Systematic Review.","authors":"Emma Sola, Jose A Morales-García, Francisco López-Muñoz, Eva Ramos, Alejandro Romero","doi":"10.3390/antiox14060712","DOIUrl":"10.3390/antiox14060712","url":null,"abstract":"<p><p>Alkylating agents, historically employed as chemical warfare agents and currently used as chemotherapeutic drugs, are known to induce significant pulmonary toxicity. Current clinical interventions often fail to fully prevent or reverse these pathological changes, highlighting the urgent need for safe, broad-spectrum therapeutic agents that are effective across diverse exposure scenarios. Melatonin has emerged as a promising protective agent due to its antioxidant, anti-inflammatory, and immunomodulatory properties, along with a well-established safety profile. This systematic review evaluates the potential of melatonin in mitigating vesicant-induced pulmonary damage, synthesizing and critically analyzing preclinical evidence in accordance with the PRISMA guidelines. Three in vivo rodent studies met the inclusion criteria and were analyzed. In all cases, melatonin demonstrated protective effects against alkylating agents such as mechlorethamine (HN2) and cyclophosphamide (CP). These effects were dose-dependent and observed across various animal models, administration protocols, and dosages (ranging from 2.5 to 100 mg/kg), highlighting the importance of context-specific considerations. The human equivalent doses (HEDs) ranged from 12 to 973 mg per day, suggesting that the effective doses may exceed those typically used in clinical trials for other conditions. Melatonin's pleiotropic mechanisms, including a reduction in oxidative stress, the modulation of inflammatory pathways, and support for tissue repair, reinforce its therapeutic potential in both prophylactic and treatment settings for alkylating agent exposure. Nonetheless, this review underscores the critical need for further randomized clinical trials to establish the optimal dosing strategies, refine treatment protocols, and fully elucidate melatonin's role in managing alkylating-agent-induced pulmonary toxicity.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493718","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":"Valorization of Food Waste: Extracting Bioactive Compounds for Sustainable Health and Environmental Solutions.","authors":"Nikša Bekavac, Korina Krog, Ana Stanić, Dunja Šamec, Anita Šalić, Maja Benković, Tamara Jurina, Jasenka Gajdoš Kljusurić, Davor Valinger, Ana Jurinjak Tušek","doi":"10.3390/antiox14060714","DOIUrl":"10.3390/antiox14060714","url":null,"abstract":"<p><p>Food waste is a major economic, environmental, and ethical challenge, as around a third of the edible food produced worldwide is lost or wasted. This inefficiency not only increases food insecurity but also results in resource depletion and environmental degradation. Dealing with food waste through sustainable management strategies, such as upcycling food by-products, has proven to be a promising approach to optimize resource use and support the circular economy. Valorization of food waste enables the extraction of valuable bioactive compounds with strong antioxidant properties. These natural antioxidants play a crucial role in mitigating diseases caused by oxidative stress, including cardiovascular diseases, neurodegenerative diseases, and diabetes. Utilizing food-derived polysaccharides as functional ingredients in the food, pharmaceutical, and cosmetics industries represents an environmentally friendly alternative to synthetic additives and is in line with global sustainability goals. Various extraction techniques, including enzymatic hydrolysis and ultrasound-assisted methods, enhance the recovery of these bioactives while preserving their structural integrity and efficacy. By integrating technological advances and sustainable practices, the food industry can significantly reduce waste while developing high-value products that contribute to human health and environmental protection. This review underscores the significance of food by-product valorization, aiming to bridge the gap between fundamental research and practical applications for a more sustainable future. The literature was selected based on scientific relevance, methodological quality, and applicability to the food, pharmaceutical, or cosmetic sectors. Studies lacking empirical data, not addressing the extraction or application of bioactives, or published in languages other than English were excluded.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493688","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":"Targeting Spermine Oxidase to Mitigate Traumatic Brain Injury Pathology in the Aging Brain.","authors":"Jui-Ming Sun, Jing-Shiun Jan, Ting-Lin Yen, Yu-Hao Chen, Ruei-Dun Teng, Chih-Hao Yang, Cheng-Ta Hsieh","doi":"10.3390/antiox14060709","DOIUrl":"10.3390/antiox14060709","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) in the elderly is frequently associated with worsened neurological outcomes and prolonged recovery, yet the age-specific molecular mechanisms driving this vulnerability remain poorly understood. Aging is characterized by increased oxidative stress and chronic neuro-inflammation, both of which may amplify the brain's susceptibility to injury. In this study, we identify spermine oxidase (SMOX), a polyamine-catabolizing enzyme that produces reactive oxygen species, as a key mediator linking oxidative stress and neuro-inflammation to age-dependent TBI susceptibility. Using a mouse model of controlled cortical impact (CCI), we found that SMOX expression was significantly upregulated in aged brains, primarily in neurons and microglia, and this increase correlated with greater microglial activation, elevated pro-inflammatory cytokine expression, and widespread neuronal degeneration. Notably, SMOX upregulation also impaired astrocytic glutamate clearance by disrupting the membrane localization of the transporter GLT-1, contributing to excitotoxic stress. Importantly, analysis of postmortem human brain samples and transcriptomic data revealed a parallel age-related increase in SMOX expression, supporting its translational relevance. The pharmacological inhibition of SMOX with JNJ-9350 in aged mice reduced oxidative and inflammatory markers, preserved neuronal viability, and improved motor, cognitive, and emotional outcomes up to 30 days post-injury. These findings establish SMOX as a critical molecular driver of age-related vulnerability to TBI and highlight its inhibition as a promising therapeutic strategy for improving outcomes in elderly TBI patients.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493704","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":"Cooperative Interaction of Hyaluronic Acid with Epigallocatechin-3-O-gallate and Xanthohumol in Targeting the NF-κB Signaling Pathway in a Cellular Model of Rheumatoid Arthritis.","authors":"Francesco Longo, Alessandro Massaro, Manuela Mauro, Mario Allegra, Vincenzo Arizza, Luisa Tesoriere, Ignazio Restivo","doi":"10.3390/antiox14060713","DOIUrl":"10.3390/antiox14060713","url":null,"abstract":"<p><p>Current intra-articular therapies with hyaluronic acid (HA) provide symptomatic relief in joint diseases, but have limited efficacy in counteracting oxidative stress and inflammation, key drivers of cartilage degradation in rheumatoid arthritis (RA). To address this limitation, the potential of combining HA with the phytochemicals xanthohumol (XAN) and epigallocatechin-3-O-gallate (EGCG), known for their antioxidant and anti-inflammatory properties, was evaluated in a cellular model of RA (SW982 synoviocytes stimulated with interleukin-1β, IL-1β). The Chou-Talalay method demonstrated that their combination synergistically reduced reactive oxygen species (ROS) and nitric oxide (NO) levels. The \"TRIPLE\" combination (HA + XAN + EGCG) showed the lowest combination index and the highest dose reduction index. Compared to individual treatments, TRIPLE significantly decreased IL-1β-induced IL-6, IL-8, TNF-α, and MMP-3 levels, while increasing the levels of the anti-inflammatory cytokine IL-10. Western blot analysis revealed a marked reduction in iNOS, COX-2, and MMP-3 protein expression following TRIPLE treatment. Moreover, the combination inhibited IL-1β-induced phosphorylation of IκB and p65, thereby preventing NF-κB activation. These findings suggest that integrating XAN and EGCG into injectable HA formulations may represent a promising strategy to improve the management of joint inflammation in RA.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493612","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":"Subchronic Intranasal Administration of NeuroEPO Reduces Long-Term Consequences of Severe Traumatic Brain Injury in Male Rats.","authors":"Félix Iván López-Preza, Maria de Los Angeles Nuñez-Lumbreras, Iliana Sosa-Testé, Alonso Fernández-Guasti, Luis Concha, Teresita Rodríguez-Obaya, Luisa Rocha","doi":"10.3390/antiox14060710","DOIUrl":"10.3390/antiox14060710","url":null,"abstract":"<p><p>Current treatments fail to prevent long-term consequences induced by a severe traumatic brain injury (TBI). This study aimed to evaluate the efficacy of repetitive intranasal administration of NeuroEPO (a derivative of erythropoietin) on long-term alterations after a severe TBI induced by the application of a lateral fluid percussion in male rats. A otal of 30-31 days after the trauma, TBI+vehicle group showed sensorimotor dysfunction (Neuroscore, <i>p</i> < 0.0009; beam walking test, <i>p</i> < 0.0001 vs. Sham+vehicle group) and depressive-like behavior suggested by increased immobility (<i>p</i> = 0.0009 vs. baseline) during the forced swim test. Rats also showed increased production of malondialdehyde (a marker of oxidative damage), increased catalase activity (an antioxidant enzyme), and atrophy of brain areas evaluated with Magnetic Resonance Imaging 31 days after the trauma. TBI+NeuroEPO group received intranasal administration of NeuroEPO (0.136 mg/kg) starting 3 h post-TBI and continued every 8 h for four days. This group showed less sensorimotor dysfunction (Neuroscore, <i>p</i> = 0.020; beam walking test, <i>p</i> = 0.001, vs. TBI+vehicle group) and normal immobility behavior (<i>p</i> = 0.998 vs. Sham+vehicle group). Levels of malondialdehyde and catalase as well as the volume of brain structures of this group were like the Sham+vehicle group. These findings support the potential of NeuroEPO as a therapeutic agent to reduce long-term consequences of TBI.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493780","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":"Impact of Obesity Caused by a High-Fat Diet on the Heart's Redox Balance.","authors":"Yildy Utreras-Mendoza, Isidora Mujica Valenzuela, Luis Montecinos, Paulina Donoso, Gina Sánchez","doi":"10.3390/antiox14060708","DOIUrl":"10.3390/antiox14060708","url":null,"abstract":"<p><p>Obesity has been implicated in the induction of oxidative stress, which is thought to contribute to the pathogenesis of various cardiovascular diseases, including cardiac hypertrophy. However, the redox status during the early stages of cardiac hypertrophy remains inadequately characterized. In this study, we administered a high-fat diet (HFD) to C57BL/6N mice for 12 weeks. We investigated the expression of biomarkers associated with hypertrophy and oxidative stress, including lipid peroxidation, protein carbonylation, and the redox couples NADH/NAD⁺, NADPH/NADP⁺, and GSH/GSSG. Additionally, we assessed the expression levels and enzymatic activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase. Following 12 weeks on a HFD, mice exhibited obesity and a 10% increase in the heart weight/tibia length ratio, together with an upregulation in the mRNA levels of β-myosin heavy chain, brain natriuretic peptide, and regulator of calcineurin 1, isoform 4. There was also a significant increase in NOX4 content in the heart of these animals; however, we observed no rise in protein carbonylation and a decrease in lipid peroxidation products. As for the redox couples, the GSH/GSSG ratio nearly doubled, while the NADH/NAD⁺ and NADPH/NADP⁺ ratios remained stable. All antioxidant enzyme mRNAs examined showed increased expression; however, only glutathione reductase showed higher activity. Our findings suggest that reductive stress is predominant within the cardiac environment of these animals.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493715","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":"Natural Hydroxybenzoic and Hydroxycinnamic Acids Derivatives: Mechanisms of Action and Therapeutic Applications.","authors":"Sergio López-Herrador, Julia Corral-Sarasa, Pilar González-García, Yaco Morillas-Morota, Enrica Olivieri, Laura Jiménez-Sánchez, María Elena Díaz-Casado","doi":"10.3390/antiox14060711","DOIUrl":"10.3390/antiox14060711","url":null,"abstract":"<p><p>Hydroxybenzoic and hydroxycinnamic acid derivatives are a class of organic compounds derived from benzoic and cinnamic acid, respectively, two types of acids in which one of the hydrogen atoms on the benzene ring is replaced by a hydroxyl (-OH) or alkoxyl group (-O-R). These compounds are found in a wide range of natural sources, particularly in plants, as well as in some fungi. Their biological properties are distinctive, as they combine antioxidant, anti-inflammatory, and metabolic functions, which can be utilized for therapeutic purposes in humans. In this review, we identify the most relevant hydroxybenzoic and hydroxycinnamic acid derivatives for human applications, explain their common and specific mechanisms of action, and highlight their applications in significant preclinical and clinical studies.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493736","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}