Redox Report最新文献_第5页

Manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) represses sulfide:quinone oxidoreductase expression and targets the sulfido-redox system in glioblastoma models. 在胶质母细胞瘤模型中，锰（III）四苯甲酸卟啉（MnTBAP）抑制硫化物：醌氧化还原酶的表达并靶向硫氧化还原系统。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-09-18 DOI: 10.1080/13510002.2025.2557081

Elise Malard, Benoît Bernay, Jérôme Toutain, Samantha Ballesta, Marie Lévêque, Julien Pontin, Samuel Valable, Myriam Bernaudin, Laurent Chatre

{"title":"Manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) represses sulfide:quinone oxidoreductase expression and targets the sulfido-redox system in glioblastoma models.","authors":"Elise Malard, Benoît Bernay, Jérôme Toutain, Samantha Ballesta, Marie Lévêque, Julien Pontin, Samuel Valable, Myriam Bernaudin, Laurent Chatre","doi":"10.1080/13510002.2025.2557081","DOIUrl":"10.1080/13510002.2025.2557081","url":null,"abstract":"Background: The adaptation of the redox system and bioenergetics is a major factor contributing to cancer metabolism. Redox therapy is promising but still requires molecular studies that consider the reactive species interactome (RSI) concept, which integrates reactive oxygen, nitrogen, sulfur, carbonyl species, and redox enzymes. Our aim was to decipher the role of the RSI in glioblastoma (GBM), including by challenging the RSI with the MnTBAP redox agent.Methods: The effects of MnTBAP on the redox system and bioenergetics were investigated on several GBM models, namely in vitro 2D culture, in vitro 3D culture with two human GBM tumoroids, and in vivo preclinical model, which included male and female comparisons.Results: We show - for the first time - that MnTBAP represses the sulfide:quinone oxidoreductase (SQOR) involved in the sulfur metabolism and bioenergetics, and targets the RSI through the sulfido-redox system. Through in vitro silencing and overexpression approaches, we also demonstrate that SQOR contributed to GBM cell growth and that its decrease is involved in the molecular effect of MnTBAP. Consequently, MnTBAP induces a switch between apoptosis, uncontrolled necrosis, and ferroptosis depending on the glioblastoma models.Conclusion: Our findings represent the next step in establishing a better understanding of redox biology in the context of GBM.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2557081"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086941","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

Ultraviolet B-induced oxidative damage in human skin keratinocytes is alleviated by Pinus morrisonicola leaf essential oil through activation of the Nrf2-dependent antioxidant defense system. 松叶精油通过激活nrf2依赖的抗氧化防御系统，减轻紫外线b诱导的人皮肤角质形成细胞氧化损伤。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-02 DOI: 10.1080/13510002.2025.2527427

Wan-Teng Lin, Yi-Ju Chen, Hsin-Ning Kuo, Suresh Kumar, Mosleh Mohammad Abomughaid, K J Senthil Kumar

{"title":"Ultraviolet B-induced oxidative damage in human skin keratinocytes is alleviated by Pinus morrisonicola leaf essential oil through activation of the Nrf2-dependent antioxidant defense system.","authors":"Wan-Teng Lin, Yi-Ju Chen, Hsin-Ning Kuo, Suresh Kumar, Mosleh Mohammad Abomughaid, K J Senthil Kumar","doi":"10.1080/13510002.2025.2527427","DOIUrl":"10.1080/13510002.2025.2527427","url":null,"abstract":"Background: Ultraviolet B (UVB) radiation contributes to skin disorders such as photodamage, photoaging, and cancer. Natural antioxidants can mitigate UVB-induced damage. Pinus morrisonicola (Taiwan white pine), known for its anti-cancer, anti-inflammatory, and antioxidant properties, is used in health-promoting beverages, but its skin-protective effects remain underexplored.Purpose: This study investigates the protective effects of P. morrisonicola leaf essential oil (PMLEO) against UVB-induced damage in HaCaT keratinocytes.Methods: HaCaT cells were exposed to UVB and treated with PMLEO. Cell viability, reactive oxygen species (ROS) levels, and antioxidant enzyme expression were assessed. The role of Nrf2, a key antioxidant regulator, was evaluated through knockdown experiments. The effects on UVB-induced melanogenesis were examined via α-MSH secretion followed by p53-mediated POMC expression.Results: PMLEO and P. morrisonicola bark essential oil (PMBEO) were non-cytotoxic up to 200 µg/mL. UVB reduced cell viability to 43%, but PMLEO co-treatment significantly restored viability and reduced ROS levels via Nrf2 activation, increasing NQO-1 and HO-1. Nrf2 knockdown impaired PMLEO's protection. PMLEO also inhibited UVB-induced α-MSH secretion by downregulating p53-mediated POMC expression, suggesting an anti-melanogenic effect.Conclusion: PMLEO protects dermal keratinocytes against UVB-induced oxidative stress, cell death, and melanogenesis via Nrf2 activation, highlighting its potential as a natural skin protectant.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2527427"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12231284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144554334","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

ROS-Drp1-mitophagy feedback loop regulates myogenic differentiation via actin cytoskeleton remodeling-mediated MRTF-A/SRF axis. ros - drp1 -自噬反馈回路通过肌动蛋白细胞骨架重塑介导的MRTF-A/SRF轴调控成肌分化。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-21 DOI: 10.1080/13510002.2025.2536400

Aiwen Jiang, Luyao Wang, Xinyu Liu, Jialong Li, Haifei Wang, Shenglong Wu, Wenbin Bao

{"title":"ROS-Drp1-mitophagy feedback loop regulates myogenic differentiation via actin cytoskeleton remodeling-mediated MRTF-A/SRF axis.","authors":"Aiwen Jiang, Luyao Wang, Xinyu Liu, Jialong Li, Haifei Wang, Shenglong Wu, Wenbin Bao","doi":"10.1080/13510002.2025.2536400","DOIUrl":"10.1080/13510002.2025.2536400","url":null,"abstract":"Background: Mitochondrial division is one of the main characteristics for the initiation of myogenic differentiation. However, the role and mechanism of Dynamin-related protein 1 (Drp1), the most important protein that regulates mitochondrial fission in mammals, in regulating myogenic differentiation are not well understood.Methods: Drp1 siRNAs were transfected to C2C12 cells, or AAV9-shDrp1 were injected to C57BL/6J mice to knockdown Drp1 expression. Then, mitochondrial damage, ROS level, myogenic differentiation, mitophagy and actin/MRTF-A/SRF pathway was detected by quantitative real-time PCR, western blotting, immunofluorescence staining and flow cytometry.Results: The results showed that Drp1 was upregulated after C2C12 differentiation; Drp1 knockdown by siRNA transfection impaired myotube formation. ROS are the upstream activators for Drp1 expression, and Drp1 inversely reduces ROS by facilitating mitophagy to form a ROS-Drp1-mitophagy feedback loop during myogenic differentiation. Knockdown of Drp1 disrupted the ROS-Drp1-mitophagy feedback loop-mediated ROS homeostasis, thereby accelerating F-action depolymerization and blocking MRTF-A nuclear translocation by reducing the phosphorylation of cofilin. A decrease in MRTF-A nuclear translocation impaired SRF activity and hindered myogenic differentiation.Conclusion: In summary, this study revealed the functional mechanism of Drp1 and clarified the interactions among ROS, Drp1-mediated mitophagy and actin cytoskeleton remodeling during myogenic differentiation.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2536400"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12281654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144683018","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

Involvement of endolysosome iron in HIV-1 gp120-, morphine-, and iron supplementation-induced disruption of the reactive species interactome and induction of neurotoxicity. 内溶酶体铁参与HIV-1 gp120-、吗啡-和铁补充剂诱导反应性物种相互作用的破坏和神经毒性的诱导。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-08-21 DOI: 10.1080/13510002.2025.2546496

Nirmal Kumar, Peter W Halcrow, Darius N K Quansah, Braelyn Liang, Olimpia Meucci, Jonathan D Geiger

{"title":"Involvement of endolysosome iron in HIV-1 gp120-, morphine-, and iron supplementation-induced disruption of the reactive species interactome and induction of neurotoxicity.","authors":"Nirmal Kumar, Peter W Halcrow, Darius N K Quansah, Braelyn Liang, Olimpia Meucci, Jonathan D Geiger","doi":"10.1080/13510002.2025.2546496","DOIUrl":"https://doi.org/10.1080/13510002.2025.2546496","url":null,"abstract":"Background: Iron continues to be linked to the pathogenesis of neurodegenerative disorders including HIV-1 associated neurocognitive disorders (HAND). People with HIV-1 who use opioids have a higher risk of developing HAND, and HIV-1 proteins and opioids disrupt endolysosome iron homeostasis, increase reactive oxygen species (ROS), and cause neural cell death. Endolysosomes are subcellular acidic organelles that regulate iron metabolism and redox homeostasis. HIV-1 gp120 and opioids induce endolysosome iron release, increasing cytosolic and in mitochondrial iron and ROS and inducing neurotoxicity. However, ROS represent only part of the reactive species interactome (RSI) and little is known about the extent to which HIV-1 proteins and opioids affect the RSI.Results: In SH-SY5Y and U87MG cells, HIV-1 gp120, morphine, and iron supplementation de-acidified endolysosomes, decreased endolysosome Fe2+ and H2S, and increased ROS, lipid peroxidation (LPO) and NO. These changes were accompanied by increased cytosolic and mitochondrial Fe2+, ROS, LPO, and NO, decreased H2S, and increased cell death. All effects were blocked by the endolysosome-specific iron chelator deferoxamine.Conclusion: Endolysosome iron dyshomeostasis induced by HIV-1 gp120, morphine and iron supplementation disrupts inter-organellar iron signaling and RSI homeostasis. Targeting endolysosome iron may mitigate neurotoxicity in HAND and other disorders associated with iron overload and redox imbalance.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2546496"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12372519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966761","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

Dietary supplementation of male mice with inorganic, organic or nanoparticle selenium preparations: evidence supporting a putative gut-thyroid-male fertility axis. 雄性小鼠膳食中添加无机、有机或纳米硒制剂：支持肠道-甲状腺-雄性生育轴假说的证据。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-25 DOI: 10.1080/13510002.2025.2495367

A Mojadadi, A Au, T Ortiz Cerda, J-Y Shao, T O'Neil, K Bell-Anderson, J W Andersen, J Webb, W Salah, G Ahmad, H H Harris, P K Witting

{"title":"Dietary supplementation of male mice with inorganic, organic or nanoparticle selenium preparations: evidence supporting a putative gut-thyroid-male fertility axis.","authors":"A Mojadadi, A Au, T Ortiz Cerda, J-Y Shao, T O'Neil, K Bell-Anderson, J W Andersen, J Webb, W Salah, G Ahmad, H H Harris, P K Witting","doi":"10.1080/13510002.2025.2495367","DOIUrl":"https://doi.org/10.1080/13510002.2025.2495367","url":null,"abstract":"Selenium (Se) is linked to physiological homeostasis. Male mice (n = 8/group) were fed control (AIN93G) or diets enriched in sodium selenite (NaSe, 5.6 ppm), methylselenocysteine (Met, 4.7 ppm), diphenyl diselenide (DPDS, 14.2 ppm), or nanoselenium (NanoSe, 2.7 ppm); dietary Se ascertained by inductively-coupled plasma mass spectrometry. At 4 weeks testes, sperm, thyroids, blood and stool were collected to assess histoarchitecture, circulating hormones (thyroxine, T4; triiodothyronine, T3; thyroid stimulating hormone, TSH) and gut microbiome (16S rRNAV3-V4 amplicon sequencing). Supplemented NaSe, Met, and NanoSe increased plasma testosterone and testis glutathione peroxidases (GPx-1/4) while testicular superoxide dismutase and catalase increased slightly in the NanoSe group indicating a selective antioxidant response. Overall, NanoSe and NaSe enhanced male reproductive factors. All thyroids isolated from Se-supplemented mice contained marginal vacuoles and a lower follicle area vs control. Nano-Se enhanced thyroidiodothyronine deiodinase-1 (DIO1) expression however, thyroid GPx-1/4 remained unchanged. Supplemented NaSe and DPDSl increased plasma T3/T4 ratio, while plasma TSH was unchanged. Microbiome analyses showed that NanoSe was most efficacious in altering composition (judged by α-diversity, Shannon index and taxon richness) while the NaSe diet showed the greatest overall change in α-diversity. Dietary Se supplementation, particularly encapsulated NanoSe, may improve male fertility factors by enhancing the gut-thyroid-fertility axis.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2495367"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010115","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

Protective effects and mechanisms of cynaroside on renal fibrosis in mice with unilateral ureteral obstruction. 胞苷对单侧输尿管梗阻小鼠肾纤维化的保护作用及机制。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-05 DOI: 10.1080/13510002.2025.2500271

Ah Young Yang, Jung-Yeon Kim, Mi-Gyeong Gwon, Kiryeong Kim, Hyun Hee Kwon, Jaechan Leem, Sung-Woo Kim

{"title":"Protective effects and mechanisms of cynaroside on renal fibrosis in mice with unilateral ureteral obstruction.","authors":"Ah Young Yang, Jung-Yeon Kim, Mi-Gyeong Gwon, Kiryeong Kim, Hyun Hee Kwon, Jaechan Leem, Sung-Woo Kim","doi":"10.1080/13510002.2025.2500271","DOIUrl":"https://doi.org/10.1080/13510002.2025.2500271","url":null,"abstract":"Renal fibrosis is a key factor in the progression of chronic kidney disease (CKD), and current treatments remain inadequate. In this study, we investigated the therapeutic effects of cynaroside (Cyn), a natural flavonoid, in a mouse model of renal fibrosis induced by unilateral ureteral obstruction. Cyn treatment significantly ameliorated tubular injury and interstitial fibrosis while improving renal function. Mechanistically, Cyn inhibited the expression of fibrosis-related proteins and suppressed Smad2/3 phosphorylation. Additionally, Cyn reduced myofibroblast accumulation by inhibiting epithelial-mesenchymal transition, as indicated by increased E-cadherin expression and decreased levels of mesenchymal markers. Cyn also reduced oxidative stress by downregulating the prooxidant enzyme NADPH oxidase 4 and restoring antioxidant enzymes. Furthermore, Cyn attenuated ferroptosis by regulating key proteins, including acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, and glutathione peroxidase 4, while also restoring glutathione levels. Cyn alleviated endoplasmic reticulum stress, as evidenced by the downregulation of key markers such as glucose-regulated protein 78 and activating transcription factor 6, and reduced inflammation, as confirmed by decreased macrophage infiltration and lower cytokine production. Overall, Cyn demonstrated broad protective effects against renal fibrosis by modulating oxidative stress, ferroptosis, ER stress, and inflammation, positioning it as a potential therapeutic agent for CKD management.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2500271"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981111","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

Oxidation of human mitochondrial RNA strongly potentiates immunostimulation in an interferon-associated manner. 人线粒体RNA的氧化以干扰素相关的方式强烈增强免疫刺激。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-17 DOI: 10.1080/13510002.2025.2491845

Hung-Yun Lin, Ramon B Ramos, Dana R Crawford

{"title":"Oxidation of human mitochondrial RNA strongly potentiates immunostimulation in an interferon-associated manner.","authors":"Hung-Yun Lin, Ramon B Ramos, Dana R Crawford","doi":"10.1080/13510002.2025.2491845","DOIUrl":"https://doi.org/10.1080/13510002.2025.2491845","url":null,"abstract":"Inflammation is associated with a wide range of medical conditions, most leading causes of death, and high healthcare costs. It can thus benefit from new insights. Here we extended previous studies and found that oxidation of human native mtRNA to 'mitoxRNA' strongly potentiated IFNβ and TNFα immunostimulation in human cells, and that this newly identified type 1 interferon potentiation was transcriptional. This potentiation was significantly greater than with mtDNA oxidation, and t-butylhydroperoxide (tBHP) oxidation of RNA was more proinflammatory than hydrogen peroxide (HP). mtRNA triggered a modest increase in apoptosis that was not potentiated by oxidation, and mtDNA triggered a much greater increase. For native mtRNA, we found that chloroquine-inhibitable endosomes and MDA5 are key signaling pathways for IFNβ and TNFα production. For mitoxRNAs, RNAseq revealed a major increase in both tBHP- and HP-mitoxRNA modulated genes compared with native mtRNA. This increase was very prominent for interferon-related genes, identifying them as important mediators of this powerful oxidation effect. Moderately different gene modulations and KEGG pathways were observed for tBHP- versus HP-mitoxRNAs. These studies reveal the profound effect that mitochondrial RNA oxidation has on immunostimulation, providing new insights into DAMP inflammation and identifying potential therapeutic targets to minimize DAMP mtRNA/mitoxRNA-mediated inflammation.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491845"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008973","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

MS-275 facilitates osseointegration in osteoporotic rats by mitigating oxidative stress via activation of the miR-200a/Keap1/Nrf2 signaling pathway. MS-275通过激活miR-200a/Keap1/Nrf2信号通路减轻氧化应激，促进骨质疏松大鼠骨整合。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-02-19 DOI: 10.1080/13510002.2025.2466142

Junjie Yan, Qinsong Gu, Jianqiao Li, Zhi Zhou, Wenkai Jiang, Wengang Guan, Bin Chen, Yuhu Chen, Min Yang

{"title":"MS-275 facilitates osseointegration in osteoporotic rats by mitigating oxidative stress via activation of the miR-200a/Keap1/Nrf2 signaling pathway.","authors":"Junjie Yan, Qinsong Gu, Jianqiao Li, Zhi Zhou, Wenkai Jiang, Wengang Guan, Bin Chen, Yuhu Chen, Min Yang","doi":"10.1080/13510002.2025.2466142","DOIUrl":"10.1080/13510002.2025.2466142","url":null,"abstract":"Objectives: Osteoporosis, a prevalent metabolic bone disease affecting millions worldwide. Although MS-275 has been reported to inhibit oxidative stress, its ability to protect osteoblasts from oxidative stress damage has yet to be clarified. This study investigated whether MS-275 can inhibit oxidative stress and promote osteogenesis by activating the miRNA-200a/Keap1/Nrf2 signaling pathway.Methods: In vitro, MC3T3-E1 cells underwent induction with carbonyl cyanide 3-chlorophenylhydrazone, leading to the establishment of an oxidative stress model, investigating the underlying mechanism. In vivo, using a rat model of ovariectomized osteoporosis, evaluating the effects of MS-275.Results: In vitro, MS-275 treatment of oxidation-induced MC3T3-E1 cells resulted in up-regulation of osteoblast protein, increased expression of miRNA-200a, increased binding of miRNA-200a to Keap1 mRNA, decreased expression of Keap1 protein, and dissociation of Nrf2 from Keap1. The expressions of total Nrf2, nuclear Nrf2 and HO-1 were increased, mitochondrial function was enhanced, and oxidative damage was reduced. However, these effects were reversed after interference with miRNA-200a. In vivo,MS-275 effectively enhanced the microstructural features of distal femoral trabecular bone, increased the mineralization capacity of osteoblasts, and promoted bone formation.Discussion: MS-275 can reverse oxidative stress-induced cell damage, promote bone healing, and improve osteoporosis by activating the miRNA-200a/Keap1/Nrf2 pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2466142"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459190","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

MEGF9 prevents lipopolysaccharide-induced cardiac dysfunction through activating AMPK pathway. MEGF9通过激活AMPK通路阻止脂多糖诱导的心功能障碍。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-31 DOI: 10.1080/13510002.2024.2435252

Zhili Jin, Xianqing Li, Huixia Liu, Tao He, Wanli Jiang, Li Peng, Xiaoyan Wu, Ming Chen, Yongzhen Fan, Zhibing Lu, Di Fan, Hairong Wang

{"title":"MEGF9 prevents lipopolysaccharide-induced cardiac dysfunction through activating AMPK pathway.","authors":"Zhili Jin, Xianqing Li, Huixia Liu, Tao He, Wanli Jiang, Li Peng, Xiaoyan Wu, Ming Chen, Yongzhen Fan, Zhibing Lu, Di Fan, Hairong Wang","doi":"10.1080/13510002.2024.2435252","DOIUrl":"https://doi.org/10.1080/13510002.2024.2435252","url":null,"abstract":"Objective: Inflammation and oxidative damage play critical roles in the pathogenesis of sepsis-induced cardiac dysfunction. Multiple EGF-like domains 9 (MEGF9) is essential for cell homeostasis; however, its role and mechanism in sepsis-induced cardiac injury and impairment remain unclear.Methods: Adenoviral and adeno-associated viral vectors were applied to overexpress or knock down the expression of MEGF9 in vivo and in vitro. To stimulate septic injury, cardiomyocytes and mice were treated lipopolysaccharide (LPS). To clarify the necessity of AMP-activated protein kinase (AMPK), global AMPK knockout mice were used.Results: We found that MEGF9 expressions were reduced in cardiomyocytes and mice by LPS stimulation. Compared with negative controls, plasma MEGF9 levels were also decreased in septic patients, and negatively correlated with LPS-induced cardiac dysfunction. In addition, MEGF9 overexpression attenuated, while MEGF9 knockdown aggravated LPS-induced inflammation and oxidative damage in vivo and in vitro, thereby regulating LPS-induced cardiac injury and impairment. Mechanistic studies revealed that MEGF9 overexpression alleviated LPS-induced cardiac dysfunction through activating AMPK pathway.Conclusion: We for the first time demonstrate that MEGF9 prevents LPS-related inflammation, oxidative damage and cardiac injury through activating AMPK pathway, and provide a proof-of-concept for the treatment of LPS-induced cardiac dysfunction by targeting MEGF9.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2435252"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907569","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}

引用次数: 0

Mesenchymal stem cells enchanced by salidroside to inhibit ferroptosis and improve premature ovarian insufficiency via Keap1/Nrf2/GPX4 signaling. 红萝卜苷增强间充质干细胞通过Keap1/Nrf2/GPX4信号抑制铁凋亡并改善卵巢早衰

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-28 DOI: 10.1080/13510002.2025.2455914

Lixuan Chen, Yingnan Wu, Tiying Lv, Rui Tuo, Yang Xiao

{"title":"Mesenchymal stem cells enchanced by salidroside to inhibit ferroptosis and improve premature ovarian insufficiency via Keap1/Nrf2/GPX4 signaling.","authors":"Lixuan Chen, Yingnan Wu, Tiying Lv, Rui Tuo, Yang Xiao","doi":"10.1080/13510002.2025.2455914","DOIUrl":"10.1080/13510002.2025.2455914","url":null,"abstract":"Background: Regenerative medicine researches have shown that mesenchymal stem cells (MSCs) may be an effective treatment method for premature ovarian insufficiency (POI). However, the efficacy of MSCs is still limited.Purpose: This study aims to explain whether salidroside and MSCs combination is a therapeutic strategy to POI and to explore salidroside-enhanced MSCs inhibiting ferroptosis via Keap1/Nrf2/GPX4 signaling.Methods: The effect of salidroside and MSCs on ovarian granular cells (GCs) was analyzed. After treatment, hormone levels and -fertility of rats were measured. Lipid peroxidation levels, iron deposition and mitochondrial morphology were detected. The genes and proteins of Keap1/Nrf2/GPX4 signaling were examined.Results: Salidroside and MSCs were found to inhibit cell death of GCs by reducing peroxidation and intracellular ferrous. Salidroside promotes the proliferation of MSCs and supports cell survival in ovary. Salidroside combined with MSCs therapy restored ovarian function, which was better than MSCs monotherapy. Salidroside-enhanced MSCs to inhibit ferroptosis. The results showed activation of the Keap1/Nrf2/GPX4 signaling and an increase in anti-ferroptosis molecule.Conclusions: Salidroside-enhanced MSCs as a ferroptosis inhibitor and provide new therapeutic strategies for POI. The possible mechanisms of MSCs were related to maintaining redox homeostasis via a Keap1/Nrf2/GPX4 signaling.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2455914"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143060219","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}

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