Redox Report最新文献_第4页

Sesamin protects against Acetaminophen-induced nephrotoxicity by suppressing HMOX1-mediated apoptosis and ferroptosis. 芝麻素通过抑制hmox1介导的细胞凋亡和铁凋亡来保护对乙酰氨基酚诱导的肾毒性。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-12 DOI: 10.1080/13510002.2025.2529695

Siqi Zhu, Jingyi Ren, Yadong Zhang, Xiaoya Sun, Huanting Pei, Bowen Yin, Ziyi Wang, Zhenao Zhang, Shenghe Li, Ruonan Zhang, Ziqian Zeng, Yuxia Ma

{"title":"Sesamin protects against Acetaminophen-induced nephrotoxicity by suppressing HMOX1-mediated apoptosis and ferroptosis.","authors":"Siqi Zhu, Jingyi Ren, Yadong Zhang, Xiaoya Sun, Huanting Pei, Bowen Yin, Ziyi Wang, Zhenao Zhang, Shenghe Li, Ruonan Zhang, Ziqian Zeng, Yuxia Ma","doi":"10.1080/13510002.2025.2529695","DOIUrl":"10.1080/13510002.2025.2529695","url":null,"abstract":"Background: Acetaminophen (APAP) is a widely used antipyretic and analgesic agent, and acute exposure can lead to renal injury. Sesamin (Ses) is known for its various health benefits. However, it remains unclear whether Ses exerts a protective effect against APAP-induced kidney injury.Methods: In vivo, C57BL/6 mice were pretreated with Ses and injected intraperitoneally with APAP. In vitro, human kidney proximal tubule cells 2 were pretreated with Ses, and then models of kidney injury induced by APAP were established. Kidney damage was evaluated by morphological, inflammation, oxidative stress and protein analyzes.Results: Ses significantly improved APAP-induced nephrotoxicity in vitro and in vivo models. Transcriptomic analysis revealed that the differentially expressed genes were enriched in ferroptosis and apoptosis signaling pathways, identifying heme oxygenase 1 (HMOX1) as a core protein. In the Ses-treated group, ferroptosis and apoptosis were significantly inhibited, while HMOX1 was effectively restored. In cell experiments, both the HMOX1 agonist hemin and Ses attenuated ferroptosis and apoptosis. HMOX1 inhibitor Zinc Protoporphyrin significantly eliminated the protective effect of Ses.Conclusion: Ses alleviates APAP-induced renal injury by mediating the inhibition of ferroptosis and apoptosis via HMOX1. This study provides a new strategy for the prevention and treatment of drug-induced renal injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2529695"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12258237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619948","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

Flavonoids from Polypodium hastatum as neuroprotective agents attenuate cerebral ischemia/reperfusion injury in vitro and in vivo via activating Nrf2. 黄酮类化合物在体外和体内通过激活Nrf2减轻脑缺血再灌注损伤的作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-19 DOI: 10.1080/13510002.2024.2440204

Huankai Yao, Ruiqing Wu, Dan Du, Fengwei Ai, Feng Yang, Yan Li, Suhua Qi

{"title":"Flavonoids from Polypodium hastatum as neuroprotective agents attenuate cerebral ischemia/reperfusion injury in vitro and in vivo via activating Nrf2.","authors":"Huankai Yao, Ruiqing Wu, Dan Du, Fengwei Ai, Feng Yang, Yan Li, Suhua Qi","doi":"10.1080/13510002.2024.2440204","DOIUrl":"https://doi.org/10.1080/13510002.2024.2440204","url":null,"abstract":"Objectives: Cerebral ischemic stroke is a leading cause of death worldwide. Though timely reperfusion reduces the infarction size, it exacerbates neuronal apoptosis due to oxidative stress. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor regulating the expression of antioxidant enzymes. Activating Nrf2 gives a therapeutic approach to ischemic stroke.Methods: Herein we explored flavonoids identified from Polypodium hastatum as Nrf2 activators and their protective effects on PC12 cells injured by oxygen and glucose deprivation/restoration (OGD/R) as well as middle cerebral artery occlusion (MCAO) mice.Results: The results showed among these flavonoids, AAKR significantly improved the survival of PC12 cells induced by OGD/R and activated Nrf2 in a Keap1-dependent manner. Further investigations have disclosed AAKR attenuated oxidative stress, mitochondrial dysfunction and following apoptosis resulting from OGD/R. Meanwhile, activation of Nrf2 by AAKR was involved in the protective effects. Finally, it was found that AAKR could protect MCAO mice brains against ischemia/reperfusion injury via activating Nrf2.Discussion: This investigation could provide lead compounds for the discovery of novel Nrf2 activators targeting ischemia/reperfusion injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2440204"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865467","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

Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway. 高同型半胱氨酸血症通过抑制Nrf2/HO-1信号通路加重牙周炎。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-09 DOI: 10.1080/13510002.2025.2475691

Kaiqiang Yang, Yuting Yang, Ting Long, Xiaoxue Wang, Yeke Chen, Chenjiang He, Li Li, Xinbo Yang, Meixiu Jiang, Yichen Hu, Fang Dai, Li Song

{"title":"Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway.","authors":"Kaiqiang Yang, Yuting Yang, Ting Long, Xiaoxue Wang, Yeke Chen, Chenjiang He, Li Li, Xinbo Yang, Meixiu Jiang, Yichen Hu, Fang Dai, Li Song","doi":"10.1080/13510002.2025.2475691","DOIUrl":"10.1080/13510002.2025.2475691","url":null,"abstract":"Periodontitis, a common dental illness, causes periodontal tissue inflammation and irreversible bone loss, inevitably resulting in tooth loss. Hyperhomocysteinaemia (HHcy), defined as blood total homocysteine (Hcy) levels greater than 15 µmol/L, is linked to increased cardiovascular disease risk. Mounting evidence indicates a connection between HHcy and periodontitis; however, the underlying processes remain unknown. Herein, we explored the mechanisms by which HHcy exacerbates periodontal tissue inflammation and osteoclast formation. In an animal model of periodontitis treated with HHcy, periodontal attachment loss was aggravated, and both systemic and gingival tissue inflammation levels tended to increase; additionally, antioxidant-related proteins were suppressed and expressed at low levels, whereas oxidative damage-related protein expression increased. In RAW264.7 cells treated with LPS or LPS + Hcy, the LPS + Hcy group presented increased reactive oxygen species (ROS) fluorescence intensity, and Nrf2/HO-1 signalling pathway suppression was associated with inflammatory cytokine (TNF-α) expression. In monocyte osteoclasts treated with Rankl or Rankl + Hcy, the Rankl + Hcy group presented Nrf2/HO-1 signalling pathway suppression, an increase in osteoclast-related proteins (NFATc-1 and CTSK), and a more pronounced osteoclastic phenotype. Therefore, HHcy may exacerbate inflammation severity and osteoclast generation in periodontitis by promoting ROS production and inhibiting the Nrf2/HO-1 signalling pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2475691"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586768","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

Therapeutic combination of L-ascorbic acid, N-acetylcysteine, and dimethyl fumarate in Friedreich's ataxia: insights from in vitro models. l -抗坏血酸、n -乙酰半胱氨酸和富马酸二甲酯联合治疗弗里德赖希共济失调：来自体外模型的见解。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-15 DOI: 10.1080/13510002.2025.2505303

Fred Jonathan Edzeamey, Zenouska Ramchunder, Adamo Valle Gómez, Haobo Ge, Carlo Marya Thomas Marobbio, Charareh Pourzand, Sara Anjomani Virmouni

{"title":"Therapeutic combination of L-ascorbic acid, N-acetylcysteine, and dimethyl fumarate in Friedreich's ataxia: insights from in vitro models.","authors":"Fred Jonathan Edzeamey, Zenouska Ramchunder, Adamo Valle Gómez, Haobo Ge, Carlo Marya Thomas Marobbio, Charareh Pourzand, Sara Anjomani Virmouni","doi":"10.1080/13510002.2025.2505303","DOIUrl":"10.1080/13510002.2025.2505303","url":null,"abstract":"Friedreich's Ataxia (FRDA) is a rare neurological disorder caused by an abnormal expansion of Guanine-Adenine-Adenine (GAA) repeat in intron 1 of the FXN gene, which encodes frataxin, leading to reduced expression of frataxin, a mitochondrial protein essential for cellular homeostasis. Frataxin deficiency results in oxidative stress and mitochondrial dysfunction and impaired redox balance. Currently, there is no cure for FRDA. This study aimed to evaluate the therapeutic potential of antioxidants dimethyl fumarate (DMF), N-acetylcysteine (NAC), and L-ascorbic acid (LAA) in restoring mitochondrial redox homeostasis and frataxin levels in FRDA patient-derived fibroblasts and 2D sensory neurons. We assessed cell viability, mitochondrial and cellular reactive oxygen species (ROS) levels, mitochondrial DNA copy number, mitochondrial membrane potential, and frataxin and NRF2 expression at both mRNA and protein levels following antioxidant treatment, either individually or in combination. Treatment with LAA, NAC, and DMF resulted in significant reductions in mitochondrial and cellular ROS, along with increased FXN and NRF2 expression, and enhanced NRF2 nuclear translocation. Furthermore, these compounds improved aconitase/citrate synthase activity, GSH/GSSG ratios, and mitochondrial membrane potential. Notably, the combination of LAA and NAC consistently alleviated multiple disease-associated defects in FRDA cells, suggesting its potential as a promising therapeutic approach.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2505303"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079882","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 PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells. PKC/NOX/ROS和PYK2/MEK/ERK/PARP信号通路驱动小胶质细胞非细胞溶解性氧化应激诱导的TRPM2通道激活。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-15 DOI: 10.1080/13510002.2025.2503131

Sharifah Alawieyah Syed Mortadza, Nur Zulaikha Mohamad Zahir, Chew Tze Wei, Lin-Hua Jiang

{"title":"The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells.","authors":"Sharifah Alawieyah Syed Mortadza, Nur Zulaikha Mohamad Zahir, Chew Tze Wei, Lin-Hua Jiang","doi":"10.1080/13510002.2025.2503131","DOIUrl":"10.1080/13510002.2025.2503131","url":null,"abstract":"Objectives: The study aimed to investigate the signalling mechanism for TRPM2 channel activation by non-cytolytic oxidative stress in microglia.Methods: Microglia from wild-type (WT) and TRPM2-knockout (KO) mice were exposed to 10-30 mM H2O2 for up to 24 hours. Morphological changes characteristic of microglial activation, [Ca2+]c, ROS generation and the effects of inhibiting particular signalling pathways were examined.Results: Exposure of WT microglia to H2O2 for 24 hours caused no cell death but induced salient morphological changes, which was prevented by TRPM2-KO. Exposure of WT microglia to H2O2 to 2 hours failed, and extension to 8 hours was required, to induce an increase in [Ca2+]c, which was abolished by TRPM2-KO. Exposure of microglia to H2O2 for 8 hours induced ROS generation, which was suppressed by inhibition of PKC and NADPH oxidases (NOX). H2O2-induced PARP activation in TRPM2-KO cells was lower than that in WT cells. Furthermore, H2O2-induced activation of PARP and TRPM2 and morphological changes were attenuated by inhibition of PCK and NOX as well as PYK2 and MEK/ERK.Conclusion: Our results support that PKC/NOX-mediated ROS generation and TRPM2-mediated Ca2+-induced activation of the PYK2/MEK/ERK pathway form a positive feedback mechanism to drive TRPM2 channel activation by non-cytolytic oxidative stress.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2503131"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079879","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

Recent advances in the investigation of the regulatory network underlying reactive nitrogen species-mediated tumorigenesis: molecular mechanisms and targeted therapeutic strategies. 活性氮物种介导肿瘤发生的调控网络研究进展：分子机制和靶向治疗策略。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-10-02 DOI: 10.1080/13510002.2025.2564593

Yimao Wu, Zichang Chen, Xiaoyan Chen, Yinting Hu, Yunqi Ma

{"title":"Recent advances in the investigation of the regulatory network underlying reactive nitrogen species-mediated tumorigenesis: molecular mechanisms and targeted therapeutic strategies.","authors":"Yimao Wu, Zichang Chen, Xiaoyan Chen, Yinting Hu, Yunqi Ma","doi":"10.1080/13510002.2025.2564593","DOIUrl":"10.1080/13510002.2025.2564593","url":null,"abstract":"Reactive nitrogen species (RNS) play a pivotal role in tumorigenesis through complex regulatory networks within the tumor microenvironment (TME). This review summarizes recent advances in understanding RNS-mediated mechanisms, focusing on core components and their concentration-dependent bidirectional effects on tumor cell proliferation, apoptosis, invasion, and metabolism. It explores RNS sources in the TME, including autonomous synthesis by tumor cells and secretion by immune cells (e.g., TAMs, TANs), and their modulation of key signaling pathways (e.g., PI3 K/Akt, NF-κB, HIF-1α). Additionally, the review discusses RNS-mediated regulation of immune responses and angiogenesis, highlighting their dual roles in promoting tumor progression and enabling immune evasion. Finally, it outlines potential clinical applications, such as RNS-targeted diagnostic probes and therapeutic strategies (e.g., iNOS inhibitors, NO donors), providing a foundation for precision oncology.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2564593"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12493636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207366","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

Spermidine prevents iron overload-induced impaired bone mass by activating SIRT1/SOD2 signaling in senile rat model. 在老年大鼠模型中，亚精胺通过激活SIRT1/SOD2信号通路防止铁超载引起的骨量损伤。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-02 DOI: 10.1080/13510002.2025.2485666

Zhi-Qing Du, Jia-Bin Xie, Sheng-Yi Ji, Wanshu Zhou, Zhou-Shan Tao

{"title":"Spermidine prevents iron overload-induced impaired bone mass by activating SIRT1/SOD2 signaling in senile rat model.","authors":"Zhi-Qing Du, Jia-Bin Xie, Sheng-Yi Ji, Wanshu Zhou, Zhou-Shan Tao","doi":"10.1080/13510002.2025.2485666","DOIUrl":"10.1080/13510002.2025.2485666","url":null,"abstract":"Spermidine (SPD) is an organic compound known for its powerful antioxidant stress and anti-aging properties, and whether SPD has the ability to reduce bone mass in elderly iron overload rats is unknown. The study aimed to assess SPD's impact on iron overload-induced bone loss in elderly rats. In our aged rat model, we found that iron overload negatively influences bone metabolism and remodeling, resulting in decreased bone mineral density and increased bone loss. However, SPD treatment effectively alleviated these harmful effects, as shown by reduced serum levels of MDA and increased SOD and GSH levels. Additionally, SPD-treated rats exhibited enhanced bone mass and higher expression of OC, BMP2, SIRT1, and SOD2 in their bones. Moreover, SPD restored the imbalance in bone metabolism by counteracting the inhibition of osteogenic differentiation and promoting osteoclast differentiation induced by iron overload in MC3T3-E1 and RAW264.7 cells affected by EX527. In summary, our findings suggest that SPD's antioxidant properties may exert anti-osteoporosis effects through activation of the SIRT1/SOD2 signaling pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2485666"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11966988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773184","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

Alpha-linolenic acid protects against heatstroke-induced acute lung injury by inhibiting ferroptosis through Nrf2 activation. α -亚麻酸可通过Nrf2激活抑制铁下垂，从而预防中暑引起的急性肺损伤。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-27 DOI: 10.1080/13510002.2025.2538294

Lin Wang, Jiamin Ma, Zhaozheng Li, Xinru Zhao, Ying Chen, Pei Wang, Yi Li, Yuwei Chen, Xuanqi Yao, Liangfang Yao, Jinbao Li

{"title":"Alpha-linolenic acid protects against heatstroke-induced acute lung injury by inhibiting ferroptosis through Nrf2 activation.","authors":"Lin Wang, Jiamin Ma, Zhaozheng Li, Xinru Zhao, Ying Chen, Pei Wang, Yi Li, Yuwei Chen, Xuanqi Yao, Liangfang Yao, Jinbao Li","doi":"10.1080/13510002.2025.2538294","DOIUrl":"10.1080/13510002.2025.2538294","url":null,"abstract":"Heatstroke (HS)-induced acute lung injury (ALI) has high morbidity and mortality with no specific therapies. Ferroptosis, a form of programmed cell death driven by lipid peroxidation due to reduced Glutathione Peroxidase 4 (GPX4) activity, is closely linked to HS-induced ALI. This study investigated the effect of alpha-linolenic acid (ALA), a plant-derived ω-3 fatty acid, on ferroptosis in a mouse model of HS-induced ALI. Histopathology analysis found that ALA can attenuate lung injury and improve the 7-day survival rate in mice with HS-induced ALI. In addition, ALA significantly reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while increasing the level of antioxidant glutathione (GSH). Further analysis showed that ALA upregulated the levels of SLC7A11 and GPX4 by promoting the nuclear translocation of Nrf2. This led to increased GSH synthesis but reduced ROS accumulation, which in turn suppressed ferroptosis and protected the mice against HS-induced ALI. Additionally, the protective effect of ALA was found to be diminished in Nrf2-deficient mice. In summary, ALA inhibits ferroptosis in macrophages by activating the Nrf2/SLC7A11/GPX4 pathway and attenuates HS-induced ALI.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2538294"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12305878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733001","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

Oxidative stress activates the transplanted adipose-derived stem cells to exert antioxidant effects in alopecia treatment. 氧化应激激活移植脂肪源性干细胞在脱发治疗中发挥抗氧化作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-06-06 DOI: 10.1080/13510002.2025.2503128

Xuer Sun, Minliang Chen

{"title":"Oxidative stress activates the transplanted adipose-derived stem cells to exert antioxidant effects in alopecia treatment.","authors":"Xuer Sun, Minliang Chen","doi":"10.1080/13510002.2025.2503128","DOIUrl":"10.1080/13510002.2025.2503128","url":null,"abstract":"Background: Alopecia is a global dermatological challenge. Adipose-derived stem cells (ADSC) show therapeutic potential, but their mechanisms in promoting hair regrowth, particularly under oxidative stress conditions, remain unclear..Objective: To investigate ADSC's role in promoting hair regrowth by mitigating oxidative stress.Methods: Using H₂O₂-stressed HaCaT cells, ADSC's protective effects were evaluated via conditioned medium (CM) and co-culture. Assessments included cell viability, colony formation, ROS, MDA, antioxidant enzymes, and 8-OHdG. Nrf2 activation was analyzed by immunofluorescence and Western blot. A mouse radiation injury model validated findings.Results: Non-pretreated ADSC offered limited oxidative protection to HaCaT cells. Conversely, H₂O₂-pretreated ADSC significantly enhanced HaCaT viability and proliferation in both CM and co-culture systems. This involved paracrine activation of the Nrf2 pathway in HaCaT cells, boosting antioxidant enzymes, accelerating ROS clearance, and reducing lipid peroxidation. These effects were reversible with Nrf2 inhibition. In vivo, CM from H₂O₂-stimulated ADSC promoted hair regrowth in irradiated mice, outperforming CM from non-pretreated ADSC by activating Nrf2 and reducing tissue oxidative damage.Conclusions: Oxidative stress potentiates the protective capacity of ADSC against oxidative via Nrf2-dependent paracrine mechanisms, offering a promising strategy for alopecia treatment.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2503128"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12147514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249411","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

Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation. 去甲肾上腺素通过PKC/ nfκ b介导的NOX2上调促进血管外成纤维细胞的氧化应激。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-23 DOI: 10.1080/13510002.2025.2494314

Yi-Ming Wang, Hong-Ke Dong, Min Dai, Jing-Xiao Wang, Xiao-Yu Xu, Guo-Qing Zhu, Xiu-Zhen Li

{"title":"Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation.","authors":"Yi-Ming Wang, Hong-Ke Dong, Min Dai, Jing-Xiao Wang, Xiao-Yu Xu, Guo-Qing Zhu, Xiu-Zhen Li","doi":"10.1080/13510002.2025.2494314","DOIUrl":"https://doi.org/10.1080/13510002.2025.2494314","url":null,"abstract":"Background: Sympathetic overactivity is closely associated with vascular remodeling. Sympathetic fibers dominantly innervate the adventitia of arteries rather than tunica media. Vascular adventitial fibroblasts (VAFs) play crucial roles in vascular remodeling. However, the link between sympathetic overactivity and VAF proliferation and migration is unknown.Methods: Primary VAFs were isolated from the thoracic aorta of spontaneously hypertensive rats and Wistar-Kyoto rats. Norepinephrine (NE) bitartrate monohydrate was applied to VAFs to simulate the sympathetic overactivity.Results: NE increased NADPH oxidase (NOX) 2 expression and superoxide level, which were almost abolished by NOX2 inhibitor GSK2795039 or α-adrenoceptor antagonist prazosin, but not significantly affected by NOX1 inhibitor ML171, NOX4 inhibitor GLX351322 or β-adrenoceptor antagonist propranolol. Superoxide scavenger tempol or NOX2 inhibitor GSK2795039 attenuated NE-induced VAF proliferation and migration. NE promoted protein kinase C (PKC) phosphorylation and NFκB-p65 nuclear translocation. Either PKC inhibitor Go6983 or NFκB inhibitor BAY11-7082 attenuated NE-induced NOX activation, NOX2 upregulation, superoxide production, proliferation and migration.Conclusion: NE promotes oxidative stress by α-receptor/PKC/NFκB-mediated NOX2 upregulation, which contributes to proliferation and migration of VAFs.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2494314"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12024498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010118","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