Oxidative Medicine and Cellular Longevity最新文献

{"title":"<i>Tabernaemontana stapfiana</i> Britten (Apocynaceae) Stem Bark Prevents Alcl₃-Induced Cognitive Disability: Antioxidant and Anti-Inflammatory Activities in Wistar Rats.","authors":"Mumbi Laurantine Ngenteh, Kada Antoine Sanda, Tangu Patience Neng, Bih Belta Lilian Fubi, Ndifor Rose Nchang, Kiafon Betrand Nsah, Oumar Mahamat","doi":"10.1155/omcl/5106228","DOIUrl":"10.1155/omcl/5106228","url":null,"abstract":"<p><p>The present study aimed to evaluate the protective effects of aqueous and ethanol extracts of <i>Tabernaemontana stapfiana</i> (<i>T. stapfiana</i>) on cognitive disability induced by aluminum chloride (AlCl₃) in Wistar rats. Forty-five Wistar rats were distributed in different groups of five animals each. Test groups were daily given AlCl₃ (100 mg/kg) following by the doses of the extracts for 21 days. At the end of treatment period, rats were sacrificed and the brain homogenate and serum were prepared and used to evaluate oxidative stress in brain and serum cytokines using colorimetric tests and ELISA, respectively. The findings of this study showed that reduced brain, body weight, and antioxidant enzymes (reduced glutathione [GSH], catalase [CAT], and superoxide dismutase [SOD]), while it increases oxidant biomarkers (malondiadehyde (MDA), nitric oxide (NO) and inflammatory cytokines (IL-10, TNF-α, IL-1β, and IL-6). Therefore, the administration of aqueous or ethanol extracts of <i>T. stapfiana</i> stem bark significantly (<i>p</i>  < 0.001) reduced the IL-10, TNF-α, IL-1β, and IL-6 levels in AlCl₃-treated rats compared to non treated rats. Moreover, the extracts significantly (<i>p</i>  < 0.001) changed the oxidant-antioxidant balance by reducing the MDA and NO levels, while increasing SOD and GSH concentrations caused and NO in AlCl₃-treated rats as compared to nontreated rats. Conclusively, aqueous or ethanol extracts of <i>T. stapfiana</i> stem bark prevented the oxidative stress and inflammation in brain, which made the brain to be not change after administration of the causative agent of cognitive impairment (CI), AlCl₃.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"5106228"},"PeriodicalIF":0.0,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144874448","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":"Molecular Mechanisms of Drug-Induced Hemolysis in G6PD Deficiency: Mechanistic Insights.","authors":"Sulaiman Paika, Matthew Machini, Mayur S Parmar","doi":"10.1155/omcl/7041213","DOIUrl":"10.1155/omcl/7041213","url":null,"abstract":"<p><p>Glucose-6-phosphate dehydrogenase (G6PD) deficiency, a prevalent enzymopathy, predisposes individuals to hemolytic anemia upon exposure to various medications. This literature review explores the molecular underpinnings of drug-induced hemolytic anemia (DIHA) in G6PD-deficient patients, focusing on dapsone, amoxicillin, and primaquine. These drugs are essential for treating infections such as leprosy and malaria. However, they can damage red blood cell (RBC) membranes through complex mechanisms distinct from traditional immune-mediated pathways. Evidence suggests that drug metabolites, such as dapsone hydroxylamine and 5-hydroxyprimaquine, induce oxidative stress and disrupt RBC membrane integrity. The band 3 protein, a critical component of the RBC cytoskeleton, emerges as a key player in this process, undergoing tyrosine phosphorylation and aggregation, leading to membrane remodeling and instability. This review underscores the need for further research to elucidate the precise molecular interactions involved in drug-induced hemolysis in G6PD deficiency. Understanding these mechanisms may pave the way for developing targeted therapies, including adjuvant treatments and novel drug formulations, to mitigate the risk of hemolytic anemia in this vulnerable population.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"7041213"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12343164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835991","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: Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9783207","DOIUrl":"https://doi.org/10.1155/omcl/9783207","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2020/7126976.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9783207"},"PeriodicalIF":0.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817236","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":"<i>E2f1</i> Overexpression Reduces Aging-Associated DNA Damage in Cultured Cerebral Endothelial Cells and Improves Cognitive Performance in Aged Mice.","authors":"Sheelu Monga, Samantha Flores, Maria Pilar Blasco-Conesa, Syed M Rahman, Brian Noh, Pedram Peesh, Bhanu Priya Ganesh, Sean P Marrelli, Louise D McCullough, Jose Felix Moruno-Manchon","doi":"10.1155/omcl/3242282","DOIUrl":"10.1155/omcl/3242282","url":null,"abstract":"<p><p>As we age, cerebral endothelial cells (CECs) are less efficient in maintaining genome integrity and accumulate DNA damage. DNA damage in the brain endothelium can lead to the impairment of the blood-brain barrier (BBB), which is a major factor in brain dysfunction and dementia. Thus, identifying factors that regulate DNA repair in the brain endothelium can prevent brain dysfunction associated with aging. E2F1 is a transcription factor that regulates the expression of genes associated with DNA repair, among other functions. We hypothesize that E2F1 is downregulated in the brain vasculature of mice with aging and that E2F1 upregulation can improve cognitive function. We found that in the brain endothelium, E2F1 was significantly less phosphorylated, which is associated with its transcriptional activity, in the brain vasculature of aged mice and cultured CEC derived from aged mice compared with those from young mice. We found that <i>E2f1</i> overexpression reduced DNA damage in cultured CEC, and targeting the brain vasculature to overexpress <i>E2f1</i> improved cognition and increased the expression of genes associated with BBB integrity in aged mice. From RNA sequencing data from cultured CEC, we found that <i>E2f1</i> overexpression significantly upregulated <i>Acod1</i>, which codes for aconitate decarboxylase-1 (ACOD1), an enzyme that produces itaconate. We also found that 4-octyl itaconate (4-OI), a derivative of itaconate, reduced DNA damage, promoted cell proliferation, and restored endothelial barrier function from oxidative stress in cultured CEC. Thus, our study identifies the E2F1-ACOD1 axis as a molecular pathway that can protect the brain endothelium from oxidative stress and aging.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"3242282"},"PeriodicalIF":0.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784926","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":"Evaluating the Prophylactic and Nephroprotective Effects of Vitamin D and Metformin in Diabetic Nephropathy.","authors":"Lavanya B Ramegowda, Prashant Vishwanath, Paramahans V Salimath, Manjunath S Shetty, Srinath K Marulaiah, Shobha C Ramachandra, Akila Prashant","doi":"10.1155/omcl/5370323","DOIUrl":"10.1155/omcl/5370323","url":null,"abstract":"<p><p><b>Introduction:</b> Diabetic nephropathy (DN), a major complication of diabetes mellitus (DM) and a leading cause of end-stage renal disease (ESRD) globally, is characterized by oxidative stress (OS), chronic inflammation, and progressive fibrosis. Despite existing treatment options, disease progression remains a challenge. This study evaluates the therapeutic potential of vitamin D, alone and in combination with metformin, in mitigating DN progression in streptozotocin (STZ) induced diabetic rats. <b>Methods:</b> Male Wister rats were induced with diabetes using a single intraperitoneal injection of STZ and randomized into seven groups. Treatment regimens included vitamin D (5000 or 8000 IU), metformin (250 mg), or a combination, administered over 12 or 21 weeks. Fasting blood glucose (FBG), lipid profiles, renal function markers, and OS indicators were assessed. Renal tissues were examined via histopathological analysis to assess structural changes, and immunohistochemistry (IHC) was performed to evaluate the expression of key proteins involved in inflammation (transforming growth factor-beta [TGF-β]), fibrosis (VEGF), and OS (nuclear factor erythroid 2-related factor 2 [Nrf2]), and vitamin D receptor (VDR) signaling. <b>Results:</b> Vitamin D treatment caused a dose-dependent decrease in FBG, with the vitamin D and metformin combination therapy achieving the greatest decrease (-49.8%) by week 21. Triglyceride levels were significantly reduced (-50%), while HDL levels remained stable. Combination therapy significantly reduced hydrogen peroxide (H₂O₂) (-36.84%) and nitric oxide (NO) (-14.29%) and enhanced antioxidant enzyme activity: glutathione reductase (GR) (+250%), Superoxide dismutase (SOD) (+11.33%), and Glutathione peroxidase (GPx) (+62.83%). Histological analysis revealed preserved renal architecture and reduced fibrosis in treated groups, particularly in those receiving combination therapy. IHC showed increased VDR and Nrf2 expression, reduced VEGF and TGF-β levels, reflecting attenuation of inflammation, fibrosis, and oxidative damage. <b>Conclusion:</b> Vitamin D, particularly in combination with metformin, significantly attenuates DN progression by enhancing metabolic control, reducing OS, and preserving renal function. These findings support its potential as an effective adjunctive therapy in DN management and provide a foundation for future clinical investigations.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"5370323"},"PeriodicalIF":0.0,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12317812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775935","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":"Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet.","authors":"M Vasquez Gomez, V Filippa, M Acosta, F Mohamed, F Campo Verde, C Ferrari, G A Jahn, M S Giménez, D C Ramirez, S E Gomez Mejiba","doi":"10.1155/omcl/6334165","DOIUrl":"10.1155/omcl/6334165","url":null,"abstract":"<p><p>Mammary gland epithelial dysfunction is one of the serious consequences of subchronic dietary vitamin A deficiency (VAD). However, the underlying mechanism of this process is incompletely known. Consequently, we utilized a virgin rat model of dietary VAD (3 and 6 months) and subsequently intervened with a vitamin A sufficient (VAS) diet (0.5 or 1 month) prior to treatment completion. This experimental model allowed us to investigate the underlying molecular mechanism of mammary gland tissue dysfunction caused by VAD. Dietary VAD for 3 and 6 months caused increased inflammatory cell infiltration in the mammary gland parenchyma and glandular cells, with increased inflammation and apoptosis and reduced cell proliferation. These changes can be reversed with a VAS diet. Imbalances between the NF-κB and retinoic acid (RA) signaling pathways underlie mammary gland dysfunction following subchronic VAD. Nulliparous rats fed a VAD diet experience mammary gland epithelial dysfunction because of inflammation, apoptosis, and impaired cell growth.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"6334165"},"PeriodicalIF":0.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682893","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: Nanoscale Modification of Titanium Implants Improves Behaviors of Bone Mesenchymal Stem Cells and Osteogenesis In Vivo.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9831451","DOIUrl":"https://doi.org/10.1155/omcl/9831451","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2022/2235335.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9831451"},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12263269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144643130","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":"Erratum to \"The Role of Natural Products as Inhibitors of JAK/STAT Signaling Pathways in Glioblastoma Treatment\".","authors":"","doi":"10.1155/omcl/9876237","DOIUrl":"https://doi.org/10.1155/omcl/9876237","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2022/7838583.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9876237"},"PeriodicalIF":0.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144699213","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: Study on the Multitarget Synergistic Effects of Kai-Xin-San against Alzheimer's Disease Based on Systems Biology.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9782846","DOIUrl":"10.1155/omcl/9782846","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2019/1707218.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9782846"},"PeriodicalIF":0.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317568","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":"Eicosapentaenoic Acid (EPA) Alleviates LPS-Induced Oxidative Stress via the PPARα-NF-κB Axis.","authors":"Haya AlAbduljader, Halemah AlSaeed, Amenah Alrabeea, Ameenah Sulaiman, Mohammed J A Haider, Fahd Al-Mulla, Rasheed Ahmad, Fatema Al-Rashed","doi":"10.1155/omcl/3509596","DOIUrl":"10.1155/omcl/3509596","url":null,"abstract":"<p><p>Metabolic-endotoxemia, characterized by the translocation of lipopolysaccharide (LPS) from Gram-negative bacteria into the bloodstream, is a key contributor to chronic low-grade inflammation associated with obesity and type 2 diabetes. This condition exacerbates metabolic disruptions by activating Toll-like receptor 4 (TLR4) on macrophages, leading to the release of pro-inflammatory cytokines and subsequent insulin resistance. Eicosapentaenoic acid (EPA; C20:5 (n-3)), an omega-3 polyunsaturated fatty acid, has demonstrated anti-inflammatory and antioxidative properties, but its precise mechanisms of action in mitigating LPS-induced stress remain unclear. This study investigates the pathways through which C20:5 (n-3) alleviates LPS-induced oxidative stress and inflammation in macrophages. C20:5 (n-3) pretreatment significantly reduced LPS-induced inflammatory responses, decreasing IL-1β and IL-6 expression and IL-1β secretion, and lowering the percentage of HLA-DR⁺ macrophages. C20:5 (n-3) also attenuated ER stress, evidenced by reduced expression of ATF4, DDIT3, HSPA5/GRP78, BIP, and CHOP at both gene and protein levels. Oxidative stress was mitigated, as shown by decreased HIF1α expression, reduced ROS levels, and preservation of mitochondrial membrane potential. Importantly, C20:5 (n-3) increased the expression of PPARα and FABP5 while inhibiting NF-κB activation independently of the TLR4-IRF5 pathway. The protective effects of C20:5 (n-3) was abolished by PPARα inhibition with GW9662, indicating that C20:5 (n-3)'s action is PPARα-dependent. This study highlights the modulatory role of C20:5 (n-3) in alleviating LPS-induced oxidative stress and inflammation in macrophages through activation of the FABP5/PPARα/NF-κB axis, independently of TLR4-IRF5 signaling. These findings reveal a novel mechanism for C20:5 (n-3)'s anti-inflammatory effects and suggest that targeting the FABP5/PPARα pathway may offer therapeutic potential for treating metabolic disorders associated with chronic inflammation.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"3509596"},"PeriodicalIF":0.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317566","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}