Free Radical Research最新文献_第4页

Gold nanoparticles-supported iron oxide particles endows bone scaffolds with anti-tumor function. 金纳米颗粒-氧化铁颗粒赋予骨支架抗肿瘤功能。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-18 DOI: 10.1080/10715762.2025.2466246

Tiantian He, Wenjing Yang, Youwen Yang, Shuping Peng, Cijun Shuai

{"title":"Gold nanoparticles-supported iron oxide particles endows bone scaffolds with anti-tumor function.","authors":"Tiantian He, Wenjing Yang, Youwen Yang, Shuping Peng, Cijun Shuai","doi":"10.1080/10715762.2025.2466246","DOIUrl":"10.1080/10715762.2025.2466246","url":null,"abstract":"Iron oxide (Fe-O) has anti-tumor properties, due to its ability of catalyzing hydrogen peroxide (H2O2) of tumor cells to generate reactive oxygen species (ROS) and then cause ferroptosis. Its anti-tumor performance is restricted due to insufficient H2O2 in tumor cells. A nanomedicine, Au nanoparticles (NPs) grown on Fe-O, was integrated into poly-l-lactide (PLLA) scaffolds. Results indicated that Au NPs could consume glucose of tumor cells to produce H2O2, which supplemented reaction substrate. PLLA/Au@Fe-O scaffold showed enhanced anti-tumor activities against MG63, including increased mortality, decreased migration and colony formation. PLLA/Au@Fe-O scaffold promoted ferroptosis in MG63, including up-regulation of COX-2 protein, down-regulation of FTH1 protein and GPX4 protein. PLLA/Au@Fe-O scaffold also promoted autophagy in MG63, including down-regulation of P62 protein, and up-regulation of LC3BII/I. Mechanistically, PLLA/Au@Fe-O scaffold possessed enhanced anti-tumor activities through promoting ferroptosis and autophagy.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"169-182"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Hyper-energy metabolism of oxidative phosphorylation and enhanced glycolysis contributes to radioresistance in glioma cells. 氧化磷酸化的高能量代谢和糖酵解的增强有助于胶质瘤细胞的辐射抗性。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-01-28 DOI: 10.1080/10715762.2025.2456740

Yogesh Rai, Ankit Kumar Tiwari, Rakesh Pandey, B S Dwarakanath, Anant Narayan Bhatt

{"title":"Hyper-energy metabolism of oxidative phosphorylation and enhanced glycolysis contributes to radioresistance in glioma cells.","authors":"Yogesh Rai, Ankit Kumar Tiwari, Rakesh Pandey, B S Dwarakanath, Anant Narayan Bhatt","doi":"10.1080/10715762.2025.2456740","DOIUrl":"10.1080/10715762.2025.2456740","url":null,"abstract":"The concept of dual-state hyper-energy metabolism characterized by elevated glycolysis and OxPhos has gained considerable attention during tumor growth and metastasis in different malignancies. However, it is largely unknown how such metabolic phenotypes influence the radiation response in aggressive cancers. Therefore, the present study aimed to investigate the impact of hyper-energy metabolism (increased glycolysis and OxPhos) on the radiation response of a human glioma cell line. Modulation of the mitochondrial electron transport chain was carried out using a 2,4-dinitrophenol (DNP). Metabolic characterization was carried out by assessing glucose uptake, lactate production, mitochondrial mass, membrane potential, and ATP production. The radiation response was examined by cell growth, clonogenic survival, and cell death assays. Macromolecular oxidation was assessed by DNA damage, lipid peroxidation, and protein carbonylation assay. Hypermetabolic OPM-BMG cells exhibited a significant increase in glycolysis and OxPhos following irradiation as compared to the parental BMG-1 cells. Enhanced radioresistance of OPM-BMG cells was evidenced by the increase in α/β ratio (9.58) and D1 dose (4.18 Gy) as compared to 4.36 and 2.19 Gy in BMG-1 cells respectively. Moreover, OPM-BMG cells were found to exhibit increased resistance against radiation-induced cell death, and macromolecular oxidation as compared to BMG-1 cells. Inhibition of glycolysis and mitochondrial complex-II significantly enhanced the radiosensitivity of OPM-BMG cells compared to BMG-1 cells. Our results demonstrate that the hyper-energy metabolism of increased glycolysis and OxPhos confer radioresistance. Consequently targeting glycolysis and OxPhos in combination with radiation may overcome therapeutic resistance in aggressive cancers like glioma.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"117-128"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Nitric oxide is an irreversible human diamine oxidase inhibitor. 一氧化氮是一种不可逆的人二胺氧化酶抑制剂。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-03-08 DOI: 10.1080/10715762.2025.2465277

Felix Kosta, Elisabeth Gludovacz, Rudolf Figl, Nicole Borth, Bernd Jilma, Thomas Boehm

{"title":"Nitric oxide is an irreversible human diamine oxidase inhibitor.","authors":"Felix Kosta, Elisabeth Gludovacz, Rudolf Figl, Nicole Borth, Bernd Jilma, Thomas Boehm","doi":"10.1080/10715762.2025.2465277","DOIUrl":"10.1080/10715762.2025.2465277","url":null,"abstract":"Diamine oxidase (DAO) histamine-degradation rates are compromised in plasma of mastocytosis patients during severe mast cell activation events. Mast cell-liberated histamine induces the release of nitric oxide (NO) close to DAO extracellular storage sites. We hypothesized that NO inhibits DAO activity. Recombinant human DAO activity was measured after incubation with NO-releasing NONOates (R1R2N-(NO-)-N = O). Topaquinone reactivity was quantified by absorption measurements and by mass spectrometry. Several murine models of NO-production were assessed for DAO activity inhibition in vivo. Nitric oxide released from NONOates dose dependently and irreversibly inhibited DAO activity. The NO scavengers Trolox (Vitamin E derivative) and 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (C-PTIO), the reversible DAO inhibitors diminazene and ciproxifan, the substrates histamine (EC50 = 32 µM) and putrescine (EC50 = 39 µM), heparin whole blood and plasma protected DAO from inhibition. Nitric oxide reduced the reactivity of topaquinone to phenylhydrazine by 90%. None of the NO producing in vivo models showed DAO inhibition in plasma or tissue. Nitric oxide is a potent irreversible DAO inhibitor in vitro representing the first discovered natural inhibitor for this enzyme. Endogenous mouse DAO inhibition in vivo could not be demonstrated. The true nature of human DAO activity inhibition during severe mastocytosis events remains unknown.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"138-151"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Tetrahydrocurcumin exhibits neuroprotective effects by inhibiting neuron ferroptosis via activity of iPLA2β/p38 MAPK phosphorylation in rat TBI model. 在大鼠TBI模型中，四氢姜黄素通过iPLA2β/p38 MAPK磷酸化活性抑制神经元铁凋亡，显示出神经保护作用。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-19 DOI: 10.1080/10715762.2025.2465282

Yonghong Bi, Lan Luo, Pengyu Duan, Zhehao Jin, Xiaoqian Zhang, Guanghui He, Xiaoyan Li, Weiyu Feng, Bing Zhang

{"title":"Tetrahydrocurcumin exhibits neuroprotective effects by inhibiting neuron ferroptosis via activity of iPLA2β/p38 MAPK phosphorylation in rat TBI model.","authors":"Yonghong Bi, Lan Luo, Pengyu Duan, Zhehao Jin, Xiaoqian Zhang, Guanghui He, Xiaoyan Li, Weiyu Feng, Bing Zhang","doi":"10.1080/10715762.2025.2465282","DOIUrl":"10.1080/10715762.2025.2465282","url":null,"abstract":"Ferroptosis characterized by iron-dependent lipid peroxidation induced by traumatic brain injury (TBI) is an important factor that aggravates diseases. Studies have shown that tetrahydrocurcumin (THC) has neuroprotective effects in brain injury. However, whether THC inhibits neurocyte ferroptosis after TBI and its mechanism remains unclear. To investigate this, a weight-drop model in rats and H2O2 induced oxidative stress model in SH-SY5Y cells were established, and THC was used for treatment. Immunohistochemical staining showed that iron deposition reached its peak at 8th day after TBI. We found that THC remarkably inhibited iron accumulation in the cortical cortex and corpus callosum, improved neurological damage, reduced acute cerebral edema, weight loss, oxidative stress, and inflammation. Furthermore, the activity of iPLA2β was significantly reduced, and phosphorylation of p38 was increased after TBI, while THC alleviated the decrease in iPLA2β activity and increase in the level of P-p38. It confirmed that THC effectively mitigated ferroptosis, while iPLA2β inhibitor s-BEL could reverse the effects of THC on ferroptosis in vivo and in vitro experiments. In addition, SB202190 which is an inhibitor of p38 could enhance THC protection and lessen formation of ferroptosis-related proteins in cells. In conclusion, these findings suggested that THC may promote neurological function recovery after TBI by inhibiting neuron ferroptosis via activity of iPLA2β/P-p38.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"152-168"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Carboxymethylnaringenin: a promising antioxidant in the aqueous physiological environment. 羧甲基柚皮素：一种在水生理环境中很有前途的抗氧化剂。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-14 DOI: 10.1080/10715762.2025.2466685

Quan V Vo, Nguyen Thi Hoa, Adam Mechler

{"title":"Carboxymethylnaringenin: a promising antioxidant in the aqueous physiological environment.","authors":"Quan V Vo, Nguyen Thi Hoa, Adam Mechler","doi":"10.1080/10715762.2025.2466685","DOIUrl":"10.1080/10715762.2025.2466685","url":null,"abstract":"The synthetic naringenin derivative (2S)-8-carboxymethylnaringenin (CMN) was developed for the treatment of bacterial and viral respiratory infections. There are indications that CMN may act as an antioxidant, however, no studies have been conducted in this regard. This work is aimed at assessing the antiradical capacity of CMN against various physiologically relevant species in physiological environments by using thermodynamic and kinetic calculations. According to the results, CMN only exhibits modest HOO• antiradical activity in lipid medium, modeled here as pentyl ethanoate solvent, with an overall rate constant (koverall) of 2.01 × 102 M-1 s-1. However, significant antiradical activity is predicted for the aqueous medium (koverall = 2.60 × 105 M-1s-1) that is equivalent to the activity of the reference antioxidant Trolox. In a screen performed on a range of radicals, HO•, NO2, SO4•-, N3•, CH3O•, CCl3O•, CH3OO•, and CCl3OO• were also successfully scavenged by CMN in water at physiological pH. Therefore, other than a potent drug, CMN is also a good antioxidant in polar environments.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"183-189"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Effect of repeated sprint training in hypoxia on acute and chronic redox balance modulation. 缺氧条件下重复短跑训练对急慢性氧化还原平衡调节的影响。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-22 DOI: 10.1080/10715762.2024.2443609

M Chambion-Diaz, R Faiss, V Pialoux, G P Millet

{"title":"Effect of repeated sprint training in hypoxia on acute and chronic redox balance modulation.","authors":"M Chambion-Diaz, R Faiss, V Pialoux, G P Millet","doi":"10.1080/10715762.2024.2443609","DOIUrl":"10.1080/10715762.2024.2443609","url":null,"abstract":"Little is known regarding the effects high-intensity training performed in hypoxia on the oxidative stress and antioxidant systems. The aim of this study was to assess the potential effect of 4 weeks of repeated sprint training in hypoxia (RSH) on the redox balance. Forty male well-trained cyclists were matched into two different interventions (RSH, n = 20) or in normoxia, RSN, n = 20) and tested twice (before (Pre-) and after (Post-) a 4-week of training) for performance (repeated sprint ability (RSA) test), oxidative stress, and antioxidant status. Antioxidant enzyme activity (Superoxide Dismutase, Glutathione Peroxidase, and catalase), NO metabolites (NOx: nitrites and nitrates), ferric reducing antioxidant power, Malondialdehyde (MDA), nitrotyrosine, and carbonyls were measured in plasma. At Post-, MDA, and carbonyls increased (p < 0.05) in the RSN group both at rest (+90.6%) and also acutely in response to RSA (+22.9%); but not in RSH. At Post-, in the RSH group, catalase increased (p < 0.05) both at rest (+44.7%) and in response to the RSA test (+66.3%). At Post-, SOD, and nitrotyrosine decreased after RSA and at rest, regardless of the group (p = 0.0012 and p = 0.0413, respectively). At Post-, NOx decreased after the RSA test, regardless of the group (p < 0.05). In conclusion, several weeks of RSH training limits the increase in oxidative stress markers both at rest and in response to RSA test. Moreover, such training downregulated SOD activity, possibly due to an overproduction of reactive oxygen species. These findings could constitute a paradigm shift with a better enzymatic adaptation after RSH concomitant with a distinct reactive oxygen species (ROS) production between RSH and RSN.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-8"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Hyperoxia induces autophagy in pulmonary epithelial cells: insights from in vivo and in vitro experiments. 高氧诱导肺上皮细胞自噬：来自体内和体外实验的见解。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-02 DOI: 10.1080/10715762.2024.2446321

Kuo-Tsang Huang, Wen-Hui Tsai, Chih-Wei Chen, Yea-Shwu Hwang, Hung-Chi Cheng, Chin-Wei Yeh, Yuan-Ho Lin, An-Jie Cheng, Hao-Chun Chang, Shio-Jean Lin, Meng-Chi Yen, Wen-Tsan Chang

{"title":"Hyperoxia induces autophagy in pulmonary epithelial cells: insights from in vivo and in vitro experiments.","authors":"Kuo-Tsang Huang, Wen-Hui Tsai, Chih-Wei Chen, Yea-Shwu Hwang, Hung-Chi Cheng, Chin-Wei Yeh, Yuan-Ho Lin, An-Jie Cheng, Hao-Chun Chang, Shio-Jean Lin, Meng-Chi Yen, Wen-Tsan Chang","doi":"10.1080/10715762.2024.2446321","DOIUrl":"10.1080/10715762.2024.2446321","url":null,"abstract":"Patients with hypoxemia require high-concentration oxygen therapy. However, prolonged exposure to oxygen concentrations 21% higher than physiological concentrations (hyperoxia) may cause oxidative cellular damage. Pulmonary alveolar epithelial cells are major targets for hyperoxia-induced oxidative stress. In this study, we evaluated the therapeutic potential of the antioxidant N-acetyl-L-cysteine (NAC) for preventing hyperoxia-induced cell death. In vitro experiments were performed using the human lung cancer cell line A549. In brief, NAC-treated and untreated cells were exposed to various concentrations of oxygen (hyperoxia) for different durations. The results indicated that hyperoxia inhibited proliferation and caused cell cycle arrest in A549 cells. It also induced necrosis and autophagy. Furthermore, hyperoxia increased intracellular reactive oxygen species levels and altered mitochondrial membrane potential. Co-treatment with NAC improved the survival of cells exposed to 95% oxygen for 24 h. Experiments performed using a neonatal rat model of acute lung injury confirmed that hyperoxia induced an autophagic response. This study provides evidence for hyperoxia-induced autophagy both in vitro and in vivo. NAC can protect A549 cells from death induced by short-term hyperoxia. Our findings may inform protective strategies against hyperoxia-induced injury in developing lungs-for example, bronchopulmonary dysplasia in premature infants.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"9-22"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Anti-oxidants as therapeutic agents for oxidative stress associated pathologies: future challenges and opportunities. 抗氧化剂作为氧化应激相关病理的治疗剂：未来的挑战和机遇。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-10 DOI: 10.1080/10715762.2025.2450504

Shivani R Nandha, Rahul Checker, Raghavendra S Patwardhan, Deepak Sharma, Santosh K Sandur

{"title":"Anti-oxidants as therapeutic agents for oxidative stress associated pathologies: future challenges and opportunities.","authors":"Shivani R Nandha, Rahul Checker, Raghavendra S Patwardhan, Deepak Sharma, Santosh K Sandur","doi":"10.1080/10715762.2025.2450504","DOIUrl":"10.1080/10715762.2025.2450504","url":null,"abstract":"Free radicals have been implicated in the pathogenesis of cancer along with cardiovascular, neurodegenerative, pulmonary and inflammatory disorders. Further, the relationship between oxidative stress and disease is distinctively established. Clinical trials using anti-oxidants for the prevention of disease progression have indicated some beneficial effects. However, these trials failed to establish anti-oxidants as therapeutic agents due to lack of efficacy. This is attributed to the fact that living systems are under dynamic redox control wherein their redox behavior is compartmentalized and simple aggregation of redox couples, distributed throughout the system, is of miniscule importance while determining their overall redox state. Further, free radical metabolism is intriguingly complex as they play plural roles segregated in a spatio-temporal manner. Depending on quality, quantity and site of generation, free radicals exhibit beneficial or harmful effects. Use of nonspecific, non-targeted, general ROS scavengers lead to systemic elimination of all types of ROS and interferes in cellular signaling. Failure of anti-oxidants to act as therapeutic agents lies in this oversimplification of extremely dynamic cellular redox environment as a static and non-compartmentalized redox state. Rather than generalizing the term \"oxidative stress\" if we can identify the \"type of oxidative stress\" in different types of diseases, a targeted and more specific anti-oxidant therapy may be developed. In this review, we discuss the concept of redox dynamics, role and type of oxidative stress in disease conditions, and current status of anti-oxidants as therapeutic agents. Further, we probe the possibility of developing novel, targeted and efficacious anti-oxidants with drug-like properties.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"61-85"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

NADPH oxidase derived ROS promote arterial contraction in early postnatal rats by activation of L-type voltage-gated Ca²⁺ channels. NADPH氧化酶衍生的ROS通过激活l型电压门控Ca2+通道促进出生后早期大鼠动脉收缩。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2024-12-30 DOI: 10.1080/10715762.2024.2448483

Anastasia A Shvetsova, Valentina S Shateeva, Margarita A Khlystova, Yulia A Makukha, Olga S Tarasova, Dina K Gaynullina

{"title":"NADPH oxidase derived ROS promote arterial contraction in early postnatal rats by activation of L-type voltage-gated Ca2+ channels.","authors":"Anastasia A Shvetsova, Valentina S Shateeva, Margarita A Khlystova, Yulia A Makukha, Olga S Tarasova, Dina K Gaynullina","doi":"10.1080/10715762.2024.2448483","DOIUrl":"10.1080/10715762.2024.2448483","url":null,"abstract":"Reactive oxygen species (ROS) produced by NADPH oxidase promote contraction of peripheral arteries, which is especially pronounced in early postnatal period in comparison to adulthood, but the mechanisms of such vasomotor influence are poorly understood. We tested the hypothesis that Rho-kinase and protein kinase C (PKC) mediate procontractile influence of NADPH oxidase derived ROS in peripheral artery of early postnatal rats. In addition, we evaluated the involvement Src-kinase and L-type voltage-gated Ca2+ channels (LTCC) into procontractile influence of ROS, produced by NADPH oxidase, because of their known interplay with Rho-kinase and PKC pathways. Saphenous arteries from 11- to 15-day-old male rats were studied using quantitative PCR, isometric myography and lucigenin-enhanced chemiluminescence. Arterial tissue of early postnatal rats contained Nox2, Nox4, Duox1 and Duox2 mRNAs, among which Nox2 mRNA was the most abundant. Pan-NADPH oxidase inhibitor VAS2870 (10 µM) significantly reduced arterial contractile responses to methoxamine. The inhibitors of Rho-kinase (Y27632, 3 µM), PKC (GF109203X, 10 µM) and Src-kinase (PP2, 10 µM), as well as LTCC blockers (nimodipine, 0.1 µM, and verapamil, 0.1 μM) also reduced methoxamine-induced contraction. Importantly, the effect of VAS2870 persisted in the presence of Rho-kinase, PKC or Src-kinase inhibitors, but not in the presence of LTCC blocker. Notably, the blockade of LTCC did not affect either basal or NADPH-induced O2•- production. Our data show that LTCC, but not Rho-kinase, PKC or Src-kinase are involved into procontractile effect of ROS, produced by NADPH oxidase, in saphenous artery of young rats. Сalcium influx through LTCC does not activate ROS production by NADPH oxidase.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":"59 1","pages":"49-60"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Identification of narciclasine as a novel NRF2 inhibitor. 新型NRF2抑制剂水仙精的鉴定。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-15 DOI: 10.1080/10715762.2025.2451679

Hoang Hai Ngo, Bo-Yeung Yu, Jeong-Eun Lee, Hyunwoo Kim, Young-Sam Keum

引用次数: 0