Oxidative Medicine and Cellular Longevity最新文献

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Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet. 亚慢性维生素a缺乏饮食对初生大鼠乳腺细胞凋亡的影响。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-07-14 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/6334165
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
{"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}
引用次数: 0
RETRACTION: Nanoscale Modification of Titanium Implants Improves Behaviors of Bone Mesenchymal Stem Cells and Osteogenesis In Vivo. 撤回:纳米级钛植入物改善骨间充质干细胞的行为和体内成骨。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-07-08 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/9831451
Oxidative Medicine And Cellular Longevity
{"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}
引用次数: 0
Erratum to "The Role of Natural Products as Inhibitors of JAK/STAT Signaling Pathways in Glioblastoma Treatment". “天然产物作为JAK/STAT信号通路抑制剂在胶质母细胞瘤治疗中的作用”的勘误。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/9876237
{"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}
引用次数: 0
RETRACTION: Study on the Multitarget Synergistic Effects of Kai-Xin-San against Alzheimer's Disease Based on Systems Biology. 基于系统生物学的开心散抗阿尔茨海默病多靶点协同效应研究。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-06-10 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/9782846
Oxidative Medicine And Cellular Longevity
{"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}
引用次数: 0
Eicosapentaenoic Acid (EPA) Alleviates LPS-Induced Oxidative Stress via the PPARα-NF-κB Axis. 二十碳五烯酸(EPA)通过PPARα-NF-κB轴缓解lps诱导的氧化应激。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-06-10 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/3509596
Haya AlAbduljader, Halemah AlSaeed, Amenah Alrabeea, Ameenah Sulaiman, Mohammed J A Haider, Fahd Al-Mulla, Rasheed Ahmad, Fatema Al-Rashed
{"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<sup>+</sup> 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}
引用次数: 0
RETRACTION: Classic Prescription, Kai-Xin-San, Ameliorates Alzheimer's Disease as an Effective Multitarget Treatment: From Neurotransmitter to Protein Signaling Pathway. 摘要:经方开心散对阿尔茨海默病的多靶点治疗:从神经递质到蛋白质信号通路。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-06-10 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/9868970
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Classic Prescription, Kai-Xin-San, Ameliorates Alzheimer's Disease as an Effective Multitarget Treatment: From Neurotransmitter to Protein Signaling Pathway.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9868970","DOIUrl":"10.1155/omcl/9868970","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2019/9096409.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9868970"},"PeriodicalIF":0.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317567","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}
引用次数: 0
Ascorbic Acid Prevents Efavirenz-Induced Anxiety-Like Behavior and Brain Oxidative Stress in Zebrafish. 抗坏血酸预防斑马鱼依非韦伦诱导的焦虑样行为和大脑氧化应激。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-06-01 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/8867221
Emerson Feio Pinheiro, Norma Simone Santos da Costa, Milena Letícia Martins, Geovanna Ayami Saito, Nadyme Assad, Patrick Bruno Cardoso, Evander de Jesus Oliveira Batista, Suellen Alessandra Soares de Moraes, Adelaide da Conceição Fonseca Passos, Luana Ketlen Reis Leão, Amauri Gouveia, Karen Renata Herculano Matos Oliveira, Anderson Manoel Herculano
{"title":"Ascorbic Acid Prevents Efavirenz-Induced Anxiety-Like Behavior and Brain Oxidative Stress in Zebrafish.","authors":"Emerson Feio Pinheiro, Norma Simone Santos da Costa, Milena Letícia Martins, Geovanna Ayami Saito, Nadyme Assad, Patrick Bruno Cardoso, Evander de Jesus Oliveira Batista, Suellen Alessandra Soares de Moraes, Adelaide da Conceição Fonseca Passos, Luana Ketlen Reis Leão, Amauri Gouveia, Karen Renata Herculano Matos Oliveira, Anderson Manoel Herculano","doi":"10.1155/omcl/8867221","DOIUrl":"10.1155/omcl/8867221","url":null,"abstract":"<p><p>Efavirenz (EFV) is a medication widely used for the treatment of HIV-positive patients. Several studies have demonstrated that the prolongate use of EFV can lead to the development of neurological diseases, such as panic syndrome, depression, and anxiety disorders. In this current study, we evaluate whether the ascorbic acid (AA) treatment can prevent anxiety-like behavior and brain oxidative stress induced by EFV treatment in zebrafish. Our data demonstrated that the EFV treatment induces anxiogenic-like behavior and intense lipid peroxidation in the zebrafish brain. The AA treatment was able to prevent both anxiogenic-like behavior and brain oxidative stress elicited by the EFV treatment. Therefore, our data provide robust evidence that the EFV induced anxiety-like behavior in zebrafish via a redox-dependent pathway and that AA treatment can minimize these adverse effects. Taken together, our preclinical study strongly suggests that the use of an AA-enriched diet can minimize the effects of EFV on the central nervous system (CNS) and improve the quality of life for patients undergoing EFV treatment.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"8867221"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12145930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249031","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}
引用次数: 0
The Immunomodulatory Effect of Vitamin B12 in Pernicious Anemia: A Systematic Review. 维生素B12在恶性贫血中的免疫调节作用:一项系统综述。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-05-26 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/8463993
Tesfaye Engdaw Habtie, Alemu Birara Zemariam, Betelhem Walelgn Dagnaw, Addis Wondmagegn Alamaw, Sefineh Fenta Feleke, Molalign Aligaz Adisu
{"title":"The Immunomodulatory Effect of Vitamin B12 in Pernicious Anemia: A Systematic Review.","authors":"Tesfaye Engdaw Habtie, Alemu Birara Zemariam, Betelhem Walelgn Dagnaw, Addis Wondmagegn Alamaw, Sefineh Fenta Feleke, Molalign Aligaz Adisu","doi":"10.1155/omcl/8463993","DOIUrl":"10.1155/omcl/8463993","url":null,"abstract":"<p><p><b>Objectives:</b> The aim of this review is to draw attention to key findings from various published studies concerning the effect of methylcobalamin/cyanocobalamin on the immune response of patients diagnosed with pernicious anemia (PA). <b>Methods:</b> This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to ensure the accuracy and reliability of the included randomized controlled trials (RCTs) evaluating the impact of vitamin B12, in either natural or synthetic form, on immune function in patients with PA. The protocol was registered with PROSPERO (CRD42024518621). <b>Results:</b> Methylcobalamin/Cyanocobalamin administration in PA patients significantly increased CD3, CD8+, and CD19 cell levels, restoring them toward normal. Natural Killer (NK) cell activity improved, while the CD4/CD8 ratio decreased. These findings indicate a potential enhancement of immune function in PA patients. <b>Conclusion:</b> Significant restoration of CD3, CD8+, and CD19 cell counts was observed in PA patients after vitamin B12 administration, whether in its natural (methylcobalamin) or synthetic (cyanocobalamin) form. Additionally, NK cell activity was improved, and the CD4/CD8 ratio decreased. These findings suggest that methylcobalamin/cyanocobalamin has the potential to significantly enhance immunity in patients with PA. Therefore, we recommend conducting well-designed, large-scale Phase II and Phase III clinical trials with standardized methodologies to validate these findings and provide more robust evidence on the immunomodulatory effect of vitamin B12 in PA patients.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"8463993"},"PeriodicalIF":0.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144209089","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}
引用次数: 0
The Reactive Oxygen Species Scavenger N-Acetyl-L-Cysteine Reduces Storage-Dependent Decline in Integrin α IIb β 3-Mediated Platelet Function, Inhibiting Pre-Activation of Integrin and Its β 3 Subunit Cleavage. 活性氧清除剂n -乙酰- l-半胱氨酸抑制整合素α IIb β 3介导的血小板功能的储存依赖性下降,抑制整合素的预激活及其β 3亚基切割。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-04-21 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/7499648
Ehteramolsadat Hosseini, Zahra Beyranvand, Simone M Schoenwaelder, Fateme Farhid, Mehran Ghasemzadeh
{"title":"The Reactive Oxygen Species Scavenger N-Acetyl-L-Cysteine Reduces Storage-Dependent Decline in Integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub>-Mediated Platelet Function, Inhibiting Pre-Activation of Integrin and Its <i>β</i> <sub>3</sub> Subunit Cleavage.","authors":"Ehteramolsadat Hosseini, Zahra Beyranvand, Simone M Schoenwaelder, Fateme Farhid, Mehran Ghasemzadeh","doi":"10.1155/omcl/7499648","DOIUrl":"https://doi.org/10.1155/omcl/7499648","url":null,"abstract":"<p><p><b>Background:</b> Premature activation of integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub> plays a central role in the induction and development of the platelet storage lesion (PSL) characterized by an exhausted platelet phenotype that affects adhesion and spreading on fibrinogen. Given the role of reactive oxygen species (ROS) in regulating platelet activation per se, we investigated the effects of a ROS scavenger on reducing the functional decline of platelet integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub> during storage. <b>Methods:</b> Platelet-rich plasma-platelet concentrates (PRP-PCs) were either treated with ROS-reducing agents (1 mM N-acetyl-L-cysteine [NAC] or 30 μM NADPH oxidase [NOX] inhibitor, VAS2870) or kept untreated during storage. CD41/CD61 (total integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub>) expression and PAC-1 binding (specific to active integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub> conformation) were analyzed by flow cytometry over a 5 day storage period. Molecular changes in integrin <i>β</i> <sub>3</sub> subunit were evaluated by western blotting. Platelet adhesion/spreading to fibrinogen in the presence of ROS inhibitors was also investigated during storage using fluorescence microscopy. <b>Results:</b> A decrease in the molecular weight of integrin <i>β</i> <sub>3</sub> subunit was observed during platelet storage, and was significantly reduced by NAC but not VAS2870, suggesting proteolytic cleavage of <i>β</i> <sub>3</sub> during storage. Further to this, ROS inhibitors decreased integrin activation and increased platelet adhesion to fibrinogen from day 3 of storage, while NAC but not VAS2870 improved platelet spreading. <b>Conclusion:</b> This is the first report of increasing <i>β</i> <sub>3</sub> cleavage of integrin during storage that was inversely correlated with integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub>-mediated platelet function. In this regard, as a generic ROS scavenger, NAC was shown to reduce defects in platelet spreading through inhibition of <i>β</i> <sub>3</sub> cleavage. This is in contrast to VAS2870 which selectively inhibits cytosolic NOX alone, suggesting that the reduced platelet function observed during storage may be due to cumulative effects of mitochondrial ROS. Taken together, these studies suggest that adding NAC to platelets may significantly preserve optimal integrin <i>α</i> <sub>IIb</sub> <i>β</i> <sub>3</sub> and platelet function during storage. Moreover, as a reversible scavenger, its inhibitory effect can be readily compensated after transfusion.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"7499648"},"PeriodicalIF":0.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12048192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039256","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}
引用次数: 0
Efficacy of Plasmalogens on Monosodium Glutamate-Induced Neurotoxicity in Male Rats Through NF-κB and p38 MAPK Signaling Pathways. 缩醛磷脂通过NF-κB和p38 MAPK信号通路对谷氨酸钠诱导的雄性大鼠神经毒性的影响。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2025-04-04 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/3673280
Heba M Abdou, Fatma A Hamaad, Ghada M Abd Elmageed, Hideki Katano, Mamdooh H Ghoneum
{"title":"Efficacy of Plasmalogens on Monosodium Glutamate-Induced Neurotoxicity in Male Rats Through NF-<i>κ</i>B and p38 MAPK Signaling Pathways.","authors":"Heba M Abdou, Fatma A Hamaad, Ghada M Abd Elmageed, Hideki Katano, Mamdooh H Ghoneum","doi":"10.1155/omcl/3673280","DOIUrl":"https://doi.org/10.1155/omcl/3673280","url":null,"abstract":"<p><p>Monosodium glutamate (MSG) is the most commonly used food additive and has well-known neurotoxic effects. The current study was carried out to assess the underlying mechanisms of the neurotoxicity of MSG on the hippocampus in male rats and examine the protective effect of plasmalogens (Pls) on nuclear factor-B (NF-<i>κ</i>B) and p38 MAPK signaling pathways in the hippocampus using behavioral, biochemical, and immunohistochemical methods. Twenty-four male Wistar albino rats were divided into four groups for control or treatment with MSG (2 g/kg body weight) and/or Pls (100 mg/kg body weight). All doses were received orally for 28 days. Results show that plasmalogens ameliorate the levels of glucose, insulin, lipids, oxidative stress markers, antioxidant enzymes, AKT, and neurochemical markers. It also reduces the level of the inflammatory markers TNF-<i>α</i>, NF-<i>κ</i>B, and p38 mitogen-activated protein kinase (MAPK). Histological and immunohistochemical alterations in hippocampal tissues were found to be augmented postexposure to Pls, suggesting that Pls have a potent ameliorative effect. We conclude that Pls exert anti-inflammatory, antioxidant, and antiapoptotic effects and counteract MSG-induced neurotoxicity by altering the NF-<i>κ</i>B and p38 MAPK signaling pathways.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"3673280"},"PeriodicalIF":0.0,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004332","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}
引用次数: 0
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