Oxidative Medicine and Cellular Longevity最新文献

{"title":"The Thiol Oxidation State of Albumin Is Associated With Training Load Across an Australian Football Pre-Season.","authors":"Christopher James, Jason Weber, Corrin Boyd, Paul A Fournier, Peter G Arthur","doi":"10.1155/omcl/5534194","DOIUrl":"10.1155/omcl/5534194","url":null,"abstract":"<p><p>Australian football is a demanding contact sport where high training loads during the pre-season have been identified as a potential cause of non-contact injuries. The level of thiol-oxidised albumin, a marker of oxidative stress, might be related to the training load, and thus could be used to indirectly quantify the impact of training loads upon an athlete. The aim of this study was to investigate whether the level of thiol-oxidised albumin was affected by the pre-season training load in a team of professional Australian Football League (AFL) athletes and compare the effect of lower pre-season training loads caused by COVID-19 restrictions on the level of thiol-oxidised albumin. Forty-five participants collected daily dried blood spots in the morning prior to each training session to measure thiol-oxidised albumin using a novel methodology (OxiDx). Training load, which was operationally defined as the total distance covered during training as well as distance at certain velocities, and change of direction (COD), was measured using global positioning units. There was an association (R² = 0.12) between the level of thiol-oxidised albumin with; (1) total distance covered (p  < 0.0001), (2) distance covered at 10-20 km/h (p  < 0.0001) and 20-25 km/h (p = 0.0082) and (3) COD running (p = 0.0025). Training loads and the level of thiol-oxidised albumin were highest in the early pre-season and lowest at the conclusion of the pre-season, when training loads were reduced as a consequence of COVID-19. The measurement of the level of thiol-oxidised albumin may provide a means to indirectly quantify the impact of training loads upon an athlete, especially given the simplicity of the OxiDx methodology for fingertip blood sample collection.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e5534194"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fasciola hepatica-Derived Proteins Shield the Heart From Type 2 Myocardial Infarction in Rats by Modulating Oxidative Stress and Inflammatory Imbalance: Insights Relevant to the Hygiene Hypothesis.","authors":"Mohammadreza Ahmadi-Beni, Kobra Mokhtarian, Gholam Reza Mobini, Somayeh Najafi-Chaleshtori, Najmeh Salehi-Vanani, Maryam Anjomshoa, Fariba Houshmand","doi":"10.1155/omcl/3759583","DOIUrl":"10.1155/omcl/3759583","url":null,"abstract":"<p><p>Myocardial infarction (MI) remains a leading cause of mortality worldwide, with type 2 MI (T2MI) carrying a worse prognosis than type 1 MI (T1MI). The hygiene hypothesis suggests that reduced microbial exposure in sanitized environments contributes to immune dysregulation and inflammation-related diseases. While helminth therapy has shown potential in modulating the inflammatory responses in myocardial injury, its effects on oxidative stress remain underexplored. We hypothesize that Fasciola hepatica total protein extract (FhTE) attenuates myocardial injury in T2MI via immune modulation consistent with the hygiene hypothesis, affecting both inflammation and oxidative stress. To investigate this, male Wistar rats were pretreated with FhTE (2.5 mg/kg, intraperitoneally) daily for 6 days. MI was induced by subcutaneous isoproterenol (100 mg/kg) on days five and six. Electrocardiographic analysis 24 h post-final treatment revealed that FhTE pretreatment attenuated MI-induced changes. FhTE reduced cardiac hypertrophy and decreased serum cardiac injury markers. It enhanced antioxidant defense by increasing superoxide dismutase (SOD) and catalase (CAT) activities, lowering nitric oxide (NO) and malondialdehyde (MDA) levels, and modulating nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA levels. FhTE also reduced neutrophil and M1 macrophage activity, evidenced by decreased myeloperoxidase (MPO) levels and inducible nitric oxide synthase (iNOS) mRNA expression, and downregulated inflammatory cytokine genes (IL-1β, IL-6, TNF-⍺, and IL-33). FhTE demonstrates significant cardioprotective effects by modulating inflammation and oxidative stress, thereby preconditioning the myocardium against T2MI. These findings offer robust experimental support for the hygiene hypothesis in the context of ischemic heart disease, highlighting its potential for novel MI therapies.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e3759583"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: CO₂ Pneumoperitoneum Preserves β-Arrestin 2 Content and Reduces High Mobility Group Box-1 (HMGB-1) Expression in an Animal Model of Peritonitis.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9792742","DOIUrl":"https://doi.org/10.1155/omcl/9792742","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9792742"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147864325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological Mechanisms of Phytochemicals and Pharmaceutical Agents in Protecting Against Methotrexate-Induced Liver Injury.","authors":"Bushra Zia, Mouza Hasan Alqaishi Alshehhi, Azimullah Sheikh, Samir Mirza, Sandeep B Subramanya, Shreesh K Ojha","doi":"10.1155/omcl/9407932","DOIUrl":"10.1155/omcl/9407932","url":null,"abstract":"<p><p>Methotrexate (MTX) is a widely used chemotherapeutic and immunosuppressive agent for treating various malignancies, autoimmune diseases (AIDs), and inflammatory disorders. Despite its therapeutic efficacy, long term or high-dose MTX treatment is associated with a significant risk of hepatotoxicity, leading to MTX-induced liver injury (MTX-LI). The pathogenesis of MTX-LI involves multiple mechanisms, including oxidative stress, mitochondrial dysfunction, inflammation, and altered metabolic processes, which collectively contribute to hepatocellular damage and fibrosis. Clinically, MTX-LI manifests as elevated liver enzymes, hepatic steatosis, and, in severe cases, cirrhosis, posing a challenge to treatment regimens. To mitigate MTX-LI, a growing body of research has focused on exploring therapeutic and/or preventive potential and pharmacological mechanisms of phytochemicals and pharmaceuticals. Phytochemicals, including flavonoids, terpenoids, alkaloids, and polyphenols, exhibit hepatoprotective effects attributed to their antioxidant, anti-inflammatory, and antiapoptotic properties that can counteract MTX-induced hepatic damage. Additionally, various pharmaceutical agents possessing antioxidants and anti-inflammatory properties and favorably modulate metabolic pathways have shown promise in reducing the severity or progression of of MTX-LI. The phytochemicals or pharmaceuticals showed beneficial in MTX-LI primarily act by scavenging reactive oxygen species (ROS), modulating inflammatory pathways, and improving liver regeneration. Integrated together, its apparent that naturally occurring many phytochemicals as well as synthetic agents of pharmaceutical relevance are capable of preventing or alleviating MTX-LI. However, the optimal strategies for integrating these agents into clinical practice require further investigations to highlight safety and efficacy in humans followed by pharmacological rationale of their possible use in therapeutics. Future directions should focus on elucidating the precise molecular mechanisms, establish safety and efficacy in humans, conducting regulatory toxicology studies and randomized clinical trials, and developing combination therapies for promotion as protective agents or adjuvants to maximize efficacy and minimize adverse effects.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9407932"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13062665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Yttrium Oxide Nanoparticles Moderate the Abnormal Cognitive Behaviors in Male Mice Induced by Silver Nanoparticles\".","authors":"","doi":"10.1155/omcl/9857537","DOIUrl":"10.1155/omcl/9857537","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9857537"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Passiflora edulis f. flavicarpa Extract Prevents Muscle Atrophy and Insulin Resistance in High-Fat Diet-Induced Obese Rats via Regulating the Nrf2, NF-κB, and IRS-1/PI3K/AKT Signaling Pathways.","authors":"Nrarat Chobsuay, Pennapa Chonpathompikunlert, Jukkarin Srivilai, Wachirawadee Malakul, Nanteetip Limpeanchob, Sathid Aimjongjun, Sakara Tunsophon","doi":"10.1155/omcl/5709962","DOIUrl":"https://doi.org/10.1155/omcl/5709962","url":null,"abstract":"<p><p>High-fat diets (HFDs) are a key contributor to obesity and promote oxidative stress and inflammation, which are associated with muscle atrophy and insulin resistance (IR). Passiflora edulis exhibits anti-obesity, antioxidant, and anti-inflammatory effects. The study aimed to investigate the potential benefit of P. edulis f. flavicarpa (PF) extract in preventing obesity-associated muscle atrophy and IR. The PF extract effectively inhibited cholesterol micelle solubility with an IC₅₀ of 3431 µg/mL and decreased fat accumulation in 3T3-L1 adipocytes. Furthermore, this study investigated a model of HFD-induced IR and muscle atrophy in rats. Thirty-five male Sprague-Dawley (SD) rats were induced with obesity by HFD and were administered 250 and 500 mg/kg/day of PF extract. Rats fed with an HFD were associated with fat accumulation and oxidative stress, which promoted inflammation, muscle damage, muscle atrophy, and IR in obese rats. However, administration of PF extract effectively mitigated these effects. The PF extract decreased fat accumulation in white adipose tissues and gastrocnemius (GAS) muscle by inhibiting fat absorption and synthesis, particularly Cd36 and Hmgcr. The PF extract also notably reduced oxidative stress-induced muscle inflammation and damage via elevating nuclear factor erythroid 2-related factor 2 (Nrf2) and reducing nuclear factor kappa B (NF-κB) expressions. Additionally, PF extract was found to mechanistically prevent muscle atrophy by inhibiting Fbxo32, Trim63, and B-cell lymphoma 2 (BCL2)-associated X (Bax) expressions, while enhancing Bcl2 expression. We also found that PF extract mitigated muscle IR by upregulation of the insulin receptor substrate-1/phosphatidylinositol-3 kinase/protein kinase B (IRS-1/PI3K/AKT) pathway and Slc2a4 expression. The findings indicate that PF extract can prevent skeletal muscle loss and IR in obesity by modulating oxidative stress, inflammation, and activating IRS-1/PI3K/AKT signaling pathway.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e5709962"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESSION OF CONCERN: Neuroprotective Effect of Tea Polyphenols on Oxyhemoglobin Induced Subarachnoid Hemorrhage in Mice.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9848436","DOIUrl":"10.1155/omcl/9848436","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9848436"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Rb1 Improves Atherosclerosis by Inhibiting Endothelial Cell Pyroptosis.","authors":"Xuejiao Jiang, Tianqi Jiang, Zhaoyu Pan, Chun Chen, Xinyu Ji, Xiongyao Wang, Wenjing Zong","doi":"10.1155/omcl/6137635","DOIUrl":"10.1155/omcl/6137635","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the effect of ginsenoside Rb1 (Gs-Rb1) on endothelial cell (EC) pyroptosis in atherosclerosis (AS).</p><p><strong>Method: </strong>ApoE^-/- mice and mouse aortic endothelial cells (MAECs) were used as research subjects. An in vivo AS model was established by feeding ApoE^-/- mice a high-fat diet (HFD) for 3 months, followed by intragastric administration of Gs-Rb1 at 40 mg/kg/day for 3 months. Pathological changes were evaluated by hematoxylin-eosin (HE) and Oil Red O staining. Caspase-1 expression was detected by immunofluorescence. Pyroptosis-related protein and mRNA levels were measured by Western blotting and RT-PCR. Inflammatory factors (IL-18 and IL-1β) and LDH were quantified by ELISA. For in vitro experiments, MAECs were stimulated with oxidized low-density lipoprotein (ox-LDL, 150 μg/mL) to induce pyroptosis, followed by treatment with Gs-Rb1 (60 or 80 μg/mL) for 12 h. Cell death was assessed by flow cytometry.</p><p><strong>Result: </strong>Gs-Rb1 significantly reduced aortic plaque area in mice. It decreased the expression of pyroptosis-related proteins (caspase-1, cleaved caspase-1, GSDMD, and NLRP3) and mRNA levels in aortic tissues. Serum levels of LDH, IL-18, and IL-1β were also significantly reduced. In vitro, Gs-Rb1 reduced cell death rate and inhibited pyroptosis in endothelial cells (ECs).</p><p><strong>Conclusion: </strong>This study confirms the therapeutic effect of Gs-Rb1 on AS at both animal and cellular levels. Inhibition of EC pyroptosis may be the key mechanism underlying the anti-atherosclerotic effects of Gs-Rb1.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e6137635"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones\".","authors":"","doi":"10.1155/omcl/9857091","DOIUrl":"10.1155/omcl/9857091","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9857091"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147646054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Oxidative and Inflammatory Mechanisms Induced by Intermittent Hypoxia Leading to Vascular Alterations in Rodents: A Systematic Review and Meta-Analysis\".","authors":"","doi":"10.1155/omcl/9854762","DOIUrl":"10.1155/omcl/9854762","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9854762"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13058812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}