Redox Report最新文献_第3页

Zinc nanoparticles mitigate azoxystrobin and its nanoencapsulation-induced hepatic and renal toxicity in rats. 锌纳米颗粒减轻氮嘧菌酯及其纳米包封引起的大鼠肝、肾毒性。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-20 DOI: 10.1080/13510002.2025.2491318

Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki

{"title":"Zinc nanoparticles mitigate azoxystrobin and its nanoencapsulation-induced hepatic and renal toxicity in rats.","authors":"Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki","doi":"10.1080/13510002.2025.2491318","DOIUrl":"https://doi.org/10.1080/13510002.2025.2491318","url":null,"abstract":"This study sought to ascertain if zinc nanoparticles (ZnNPs) could lessen the toxicity of azoxystrobin (AZ). This naturally occurring methoxyacrylate is one of the most often used fungicides in agriculture in male albino rats. Six sets of 60 mature male albino rats were randomly assigned: control (distilled water), Azoxystrobin formulation (AZOF), Azoxystrobin nano-formula (AZON), ZnNPs, AZOF + ZnNPs, and AZON + ZnNPs. Blood and tissues were obtained for further immunohistochemical, pathological, and biochemical examination. The results showed that exposure to AZOF and AZON significantly increased the levels of the oxidative stress indicators glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Additionally, AZOF significantly impacts liver function bioindicators, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. AZOF and AZON induced damage to the liver and kidney by disrupting vascular dilatation and causing hemorrhages, apoptosis, inflammatory lymphocytes, and necrosis. Furthermore, co-administration of ZnNPs with fungicides (AZOF and AZON) can gently enhance the alterations of oxidative stress and liver function bioindicators levels. These findings showed that ZnNPs could help male rats receiving AZ treat their histologically abnormal liver and kidney.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491318"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996445","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

Is uric acid a true antioxidant? Identification of uric acid oxidation products and their biological effects. 尿酸是真正的抗氧化剂吗？尿酸氧化产物的鉴定及其生物学效应。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-25 DOI: 10.1080/13510002.2025.2498105

Mikaela Peglow Pinz, Isadora Medeiros, Larissa Anastácio da Costa Carvalho, Flavia Carla Meotti

{"title":"Is uric acid a true antioxidant? Identification of uric acid oxidation products and their biological effects.","authors":"Mikaela Peglow Pinz, Isadora Medeiros, Larissa Anastácio da Costa Carvalho, Flavia Carla Meotti","doi":"10.1080/13510002.2025.2498105","DOIUrl":"10.1080/13510002.2025.2498105","url":null,"abstract":"Uric acid (UA), the final product of purine metabolism in humans, exhibits a dual role as an anti or pro-oxidant, depending on the microenvironment. The two-electron oxidation of UA by biological oxidants can neutralize such harmful molecules. Additionally, UA chelates metals and can activate adaptive response against oxidation. However, some products of the reaction between UA and oxidants are not inert and, therefore, do not confer the anticipated antioxidant protection. A direct pro-oxidant effect is favoured in the one-electron oxidation of UA by heme-peroxidases yielding free radical intermediates that can initiate or propagate a radical-chain reaction. Additionally, an indirect pro-oxidant effect has been proposed by eliciting the expression or activation of enzymes that catalyse oxidant production, e.g. NADPH oxidase (NOX). This review brings together fundamental concepts and the molecular mechanisms of the redox reactions involving UA. The signature metabolites from these reactions are discussed to give valuable insights on whether these intermediates are being formed and what role they may play in disease pathogenesis. It proposes that, through identifying specific products, it may be possible to elucidate whether a harmful or protective action is linked to downstream bioactivities.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2498105"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143405","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

Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes. 线粒体功能与股骨头骨细胞骨坏死相关性的研究进展。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-18 DOI: 10.1080/13510002.2025.2491846

Chengming Li, Hangyu Ji, Suyang Zhuang, Xinhui Xie, Daping Cui, Cong Zhang

{"title":"Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes.","authors":"Chengming Li, Hangyu Ji, Suyang Zhuang, Xinhui Xie, Daping Cui, Cong Zhang","doi":"10.1080/13510002.2025.2491846","DOIUrl":"https://doi.org/10.1080/13510002.2025.2491846","url":null,"abstract":"Mitochondrial health is maintained in a steady state through mitochondrial dynamics and autophagy processes. Recent studies have identified healthy mitochondria as crucial regulators of cellular function and survival. This process involves adenosine triphosphate (ATP) synthesis by mitochondrial oxidative phosphorylation (OXPHOS), regulation of calcium metabolism and inflammatory responses, and intracellular oxidative stress management. In the skeletal system, they participate in the regulation of cellular behaviors and the responses of osteoblasts, osteoclasts, chondrocytes, and osteocytes to external stimuli. Indeed, mitochondrial damage or dysfunction occurs in the development of a few bone diseases. For example, mitochondrial damage may lead to an imbalance in osteoblasts and osteoclasts, resulting in osteoporosis, osteomalacia, or poor bone production, and chondrocyte death and inflammatory infiltration in osteoarthritis are the main causes of cartilage degeneration due to mitochondrial damage. However, the opposite exists for osteosarcoma, where overactive mitochondrial metabolism is able to accelerate the proliferation and migration of osteosarcoma cells, which is a major disease feature. Bone is a dynamic organ and osteocytes play a fundamental role in all regions of bone tissue and are involved in regulating bone integrity. This review examines the impact of mitochondrial physiological function on osteocyte health and summarizes the microscopic molecular mechanisms underlying its effects. It highlights that targeted therapies focusing on osteocyte mitochondria may be beneficial for osteocyte survival, providing a new insight for the diagnosis, prevention, and treatment of diseases associated with osteocyte death.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491846"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042067","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

CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway. CEACAM5通过JAK/ stat6依赖通路诱导气道上皮细胞铁凋亡和自噬，从而加重哮喘。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-23 DOI: 10.1080/13510002.2024.2444755

Si Liu, Li Chen, Yunxiao Shang

{"title":"CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway.","authors":"Si Liu, Li Chen, Yunxiao Shang","doi":"10.1080/13510002.2024.2444755","DOIUrl":"10.1080/13510002.2024.2444755","url":null,"abstract":"Objectives: Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology.Methods: Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse model and an IL-13-stimulated Beas-2B cell model were established for further investigation.Results: Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) was identified as a crucial gene in asthma. CEACAM5 expression was elevated in asthmatic mouse lung tissues and IL-13-stimulated Beas-2B cells, primarily in bronchial epithelial cells. CEACAM5 induced reactive oxygen species (ROS), lipid peroxidation, and ferroptosis. Interfering with CEACAM5 reduced ROS, malondialdehyde levels, and enhanced antioxidant capacity, while inhibiting iron accumulation and autophagy. Overexpression of CEACAM5 in IL-13-stimulated cells activated the JAK/STAT6 pathway, which was necessary for CEACAM5-induced autophagy, ROS accumulation, lipid peroxidation, and ferroptosis.Conclusion: CEACAM5 promotes ferroptosis and autophagy in airway epithelial cells via the JAK/STAT6 pathway, exacerbating asthma symptoms. It represents a potential target for clinical treatment.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2444755"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059975","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

Non-invasive electron paramagnetic resonance imaging detects tumor redox imbalance induced by ferroptosis. 无创电子顺磁共振成像检测由铁下垂引起的肿瘤氧化还原失衡。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-21 DOI: 10.1080/13510002.2025.2454887

Kazuhiro Kato, Hironobu Yasui, Hideo Sato-Akaba, Miho C Emoto, Hirotada G Fujii, Maciej M Kmiec, Periannan Kuppusamy, Masaki Nagane, Tadashi Yamashita, Osamu Inanami

{"title":"Non-invasive electron paramagnetic resonance imaging detects tumor redox imbalance induced by ferroptosis.","authors":"Kazuhiro Kato, Hironobu Yasui, Hideo Sato-Akaba, Miho C Emoto, Hirotada G Fujii, Maciej M Kmiec, Periannan Kuppusamy, Masaki Nagane, Tadashi Yamashita, Osamu Inanami","doi":"10.1080/13510002.2025.2454887","DOIUrl":"10.1080/13510002.2025.2454887","url":null,"abstract":"Targeting ferroptosis, cell death caused by the iron-dependent accumulation of lipid peroxides, and disruption of the redox balance are promising strategies in cancer therapy owing to the physiological characteristics of cancer cells. However, the detection of ferroptosis using in vivo imaging remains challenging. We previously reported that redox maps showing the reduction power per unit time of implanted tumor tissues via non-invasive redox imaging using a novel, compact, and portable electron paramagnetic resonance imaging (EPRI) device could be compared with tumor tissue sections. This study aimed to apply the EPRI technique to the in vivo detection of ferroptosis. Notably, redox maps reflecting changes in the redox status of tumors induced by the ferroptosis-inducing agent imidazole ketone erastin (IKE) were compared with the immunohistochemical images of 4-hydroxynonenal (4-HNE) in tumor tissue sections. Our comparison revealed a negative correlation between the reducing power of tumor tissue and the number of 4-HNE-positive cells. Furthermore, the control and IKE-treated groups exhibited significantly different distributions on the correlation map. Therefore, redox imaging using EPRI may contribute to the non-invasive detection of ferroptosis in vivo.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2454887"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143010806","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

Sodium-glucose cotransporter 2 inhibitors ameliorate glutathione cysteine ligase modifier-mediated oxidative stress and subsequent ferroptosis in proximal tubules of diabetic kidney disease. 钠-葡萄糖共转运蛋白2抑制剂改善糖尿病肾病近端小管中谷胱甘肽半胱氨酸连接酶修饰物介导的氧化应激和随后的铁下垂。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-28 DOI: 10.1080/13510002.2025.2528334

Yi-Chun Tsai, Jiun-Chi Huang, Ping-Shaou Yu, Mei-Chuan Kuo, Ling-Yu Wu, Wei-An Chang, Shang-Jyh Hwang, Ya-Ling Hsu

{"title":"Sodium-glucose cotransporter 2 inhibitors ameliorate glutathione cysteine ligase modifier-mediated oxidative stress and subsequent ferroptosis in proximal tubules of diabetic kidney disease.","authors":"Yi-Chun Tsai, Jiun-Chi Huang, Ping-Shaou Yu, Mei-Chuan Kuo, Ling-Yu Wu, Wei-An Chang, Shang-Jyh Hwang, Ya-Ling Hsu","doi":"10.1080/13510002.2025.2528334","DOIUrl":"10.1080/13510002.2025.2528334","url":null,"abstract":"Objectives: Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease. The precise molecular mechanism of ferroptosis, an iron-dependent and non-apoptotic form of regulated cell death, remains poorly understood in DKD, as does the impact of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on ferroptosis-mediated DKD.Methods: This study used bulk RNA sequencing, in vitro and in vivo models, and human kidney samples to explore the molecular mechanisms involved in oxidative stress and ferroptosis in the proximal tubule (PT) of DKD.Results: High glucose (HG) induced features of ferroptosis in HK-2 cells. Transcriptome analysis of primary PT cells from diabetic patients indicated that glutathione cysteine ligase modifier (GCLM) subunit is involved in ferroptosis. Immunohistochemical staining revealed that db/db mice and diabetic patients had lower glutathione peroxidase 4 and GCLM expression in the PT. Suppression of GCLM enhanced ferroptosis, whereas GCLM overexpression mitigated HG-induced ferroptosis in HK-2 cells. Antioxidants reduced oxidative stress and ferroptosis in both in vitro and in vivo models of DKD. Furthermore, SGLT2i attenuated PT ferroptosis in these models and improved DKD by increasing GCLM expression.Conclusion: SGLT2i reduced ferroptosis in PT by boosting GCLM expression, thereby slowing DKD progression, revealing that GCLM has the potential against DKD.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2528334"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733003","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

M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury. M6a去甲基化酶FTO在心肌缺血再灌注损伤中调控心肌细胞氧化应激、线粒体生物发生和PGC-1a稳定性。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-27 DOI: 10.1080/13510002.2025.2454892

Qiong Jiang, Xuehai Chen, Kezeng Gong, Zhe Xu, Lianglong Chen, Feilong Zhang

{"title":"M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.","authors":"Qiong Jiang, Xuehai Chen, Kezeng Gong, Zhe Xu, Lianglong Chen, Feilong Zhang","doi":"10.1080/13510002.2025.2454892","DOIUrl":"10.1080/13510002.2025.2454892","url":null,"abstract":"Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model. RT-PCR and Western blot were used to investigate the expression of the fat mass and obesity-associated (FTO) gene. Electrocardiogram, echocardiography, triphenyltetrazolium chloride (TTC) staining and hematoxylin-eosin (HE) staining were used to assess the model and the effect of FTO overexpression. The generation of reactive oxygen species (ROS) and the levels of superoxide dismutase (SOD2), mitochondrial transcription factor (TFAM) and cytochrome c oxidase I (COXI) were detected to assess the oxidative stress and mitochondrial biogenesis. RNA immunoprecipitation (RIP) and RNA pulldown assays were used to identify the interaction of FTO and PGC-1a. The m6A dot blot, methylated RNA immunoprecipitation PCR (MeRIP-PCR) and RNA stability analysis were used to analyze the regulation of methylation of PGC-1a by FTO.Results: FTO was downregulated in MIRI rats and H/R induced cardiomyocytes. Overexpression of FTO inhibited ROS level and increased the expression of SOD2, TFAM and COXI in vitro and in vivo. In addition, PGC-1a was identified as a downstream target of FTO. FTO enhanced the stability of PGC-1a mRNA through removing the m6A modification.Conclusion: Our study revealed the role of FTO regulates the oxidative stress and mitochondrial biogenesis via PGC-1a in MIRI, which may provide a new approach to mitigating MIRI.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2454892"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053451","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

Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications. 细胞色素P450 (CYP) 1酶在急性肺损伤中的作用：从分子观察到治疗意义

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-09-02 DOI: 10.1080/13510002.2025.2550807

Yiting You, Jingqian Huang, Xiaoyan Zhu, Hui Sheng, Yujian Liu

{"title":"Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications.","authors":"Yiting You, Jingqian Huang, Xiaoyan Zhu, Hui Sheng, Yujian Liu","doi":"10.1080/13510002.2025.2550807","DOIUrl":"10.1080/13510002.2025.2550807","url":null,"abstract":"Objective: This review aims to explore the roles and mechanisms of cytochrome P450 subfamily 1 (CYP1) enzymes in acute lung injury (ALI), and to discuss their potential as therapeutic targets.Methods: A comprehensive literature search was conducted using PubMed and Web of Science to identify relevant studies on the involvement of CYP1 enzymes-specifically CYP1A and CYP1B1-in various forms of ALI, including hyperoxic lung injury, sepsis-associated ALI, and COVID-19 pneumonia.Results: CYP1 enzymes, induced by the aromatic hydrocarbon receptor (AhR), contribute differentially to ALI. CYP1A enzymes exhibit protective effects, whereas CYP1B1 promotes lung injury, potentially through oxidative stress-related pathways such as Nrf2, NF-κB, and MAPK signaling.Conclusion: The distinct functions of CYP1 isoforms in ALI suggest their clinical relevance, highlighting the potential for isoform-specific targeting in the treatment of acute respiratory conditions.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2550807"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12406335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966792","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

Evaluating the anti-inflammatory and antioxidant efficacy of complementary and alternative medicines (CAM) used for management of inflammatory bowel disease: a comprehensive review. 评估用于治疗炎症性肠病的补充和替代药物（CAM）的抗炎和抗氧化功效：全面综述。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-08 DOI: 10.1080/13510002.2025.2471737

Sia Shin, Siqi Chen, Kangzhe Xie, Suehad Abou Duhun, Tamara Ortiz-Cerda

{"title":"Evaluating the anti-inflammatory and antioxidant efficacy of complementary and alternative medicines (CAM) used for management of inflammatory bowel disease: a comprehensive review.","authors":"Sia Shin, Siqi Chen, Kangzhe Xie, Suehad Abou Duhun, Tamara Ortiz-Cerda","doi":"10.1080/13510002.2025.2471737","DOIUrl":"10.1080/13510002.2025.2471737","url":null,"abstract":"Inflammatory bowel disease (IBD) is a chronic autoimmune condition whose pathogenesis has not been fully elucidated, and current treatments are not definitive and often carry several side effects. The Complementary and Alternative Medicine (CAM) offers a new approach to conventional medicine. However, their clinical application and mechanisms remain limited.Objective: The aim of this review is to evaluate the anti-inflammatory, impact on microbiota and antioxidant efficacy of currently available CAM for IBD.Methods: The literature collection was obtained from Google Scholar, MEDLINE, PubMed and Web of Science (WOS). Studies in both human and animal models, published in English language between 2018 and 2024, were selected. Sixty-seven studies were included in the current review after inclusion and exclusion screening processes.Results: Mostly, studies showed significant anti-inflammatory, gut microbiota restoring, antioxidant effects of polyphenols, polysaccharides, emodin, short-chain fatty acids (SCFA; including butyrate, propionate and acetate), and probiotics although some contrasting results were noted. Current evidence shows that polyphenols exhibit the most consistent result in alleviating IBD pathophysiology, primarily due to their significant SCFA-elevating effect.Discussion: Future studies may focus on human studies, narrowing down on individual factors which may change natural product's metabolism. Further research studies are also essential to obtain therapeutic recommendations.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2471737"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582361","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 and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies. 耳鼻咽喉疾病中的氧化应激和活性氧：从病理生理学到靶向抗氧化治疗的见解

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-02-02 DOI: 10.1080/13510002.2025.2458942

Linghui Meng, Shengyang Liu, Jinfeng Luo, Yanyi Tu, Tao Li, Ping Li, Jinzhuang Yu, Li Shi

{"title":"Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.","authors":"Linghui Meng, Shengyang Liu, Jinfeng Luo, Yanyi Tu, Tao Li, Ping Li, Jinzhuang Yu, Li Shi","doi":"10.1080/13510002.2025.2458942","DOIUrl":"10.1080/13510002.2025.2458942","url":null,"abstract":"Oxidative stress, characterized by an imbalance between excessive reactive oxygen species (ROS) production and impaired antioxidant defenses, is closely linked to the pathogenesis of various otorhinolaryngological disorders. Mitochondria, as the primary site of cellular energy production, play a crucial role in modulating oxidative stress. Mitochondrial dysfunction exacerbates ROS generation, leading to cellular damage and inflammatory responses. In otorhinolaryngological diseases, oxidative stress is strongly associated with conditions such as hearing loss, allergic rhinitis, and chronic sinusitis, where oxidative damage and tissue inflammation are key pathological features. Recent studies have highlighted the potential of antioxidant therapies to mitigate oxidative stress and restore homeostasis, offering promising avenues for alleviating symptoms in these diseases. However, despite the encouraging results from early-stage research, the clinical efficacy of antioxidant interventions remains to be fully established. This review provides an overview of the role of oxidative stress in otorhinolaryngological diseases and evaluates the therapeutic potential of antioxidant strategies.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2458942"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080986","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