Redox Report最新文献_第4页

Implication of endoplasmic reticulum stress and mitochondrial perturbations in remote liver injury after renal ischemia/reperfusion in rats: potential protective role of azilsartan. 大鼠肾缺血再灌注后内质网应激和线粒体扰动对远端肝损伤的影响：阿齐沙坦的潜在保护作用

IF 3.8 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-02-27 DOI: 10.1080/13510002.2024.2319963

Rania A Elrashidy, Esraa M Zakaria, Rehab A Hasan, Asmaa M Elmaghraby, Dina A Hassan, Ranya M Abdelgalil, Shaimaa R Abdelmohsen, Amira M Negm, Azza S Khalil, Ayat M S Eraque, Reem M Ahmed, Walaa S Sabbah, Ahmed A Ahmed, Samah E Ibrahim

{"title":"Implication of endoplasmic reticulum stress and mitochondrial perturbations in remote liver injury after renal ischemia/reperfusion in rats: potential protective role of azilsartan.","authors":"Rania A Elrashidy, Esraa M Zakaria, Rehab A Hasan, Asmaa M Elmaghraby, Dina A Hassan, Ranya M Abdelgalil, Shaimaa R Abdelmohsen, Amira M Negm, Azza S Khalil, Ayat M S Eraque, Reem M Ahmed, Walaa S Sabbah, Ahmed A Ahmed, Samah E Ibrahim","doi":"10.1080/13510002.2024.2319963","DOIUrl":"10.1080/13510002.2024.2319963","url":null,"abstract":"Objectives: Distant liver injury is a complication of renal ischemia-reperfusion (I/R) injury, which imposes mortality and economic burden. This study aimed to elucidate the cross-talk of endoplasmic reticulum (ER) stress and mitochondrial perturbations in renal I/R-induced liver injury, and the potential hepatoprotective effect of azilsartan (AZL).Methods: Male albino Wister rats were pre-treated with AZL (3 mg/kg/day, PO) for 7 days then a bilateral renal I/R or sham procedure was performed. Activities of liver enzymes were assessed in plasma. The structure and ultra-structure of hepatocytes were assessed by light and electron microscopy. Markers of ER stress, mitochondrial biogenesis and apoptosis were analyzed in livers of rats.Results: Renal ischemic rats showed higher plasma levels of liver enzymes than sham-operated rats, coupled with histological and ultra-structural alterations in hepatocytes. Mechanistically, there was up-regulation of ER stress markers and suppression of mitochondrial biogenesis-related proteins and enhanced apoptosis in livers of renal ischemic rats. These abnormalities were almost abrogated by AZL pretreatment.Discussion: Our findings uncovered the involvement of mitochondrial perturbations, ER stress and apoptosis in liver injury following renal I/R, and suggested AZL as a preconditioning strategy to ameliorate remote liver injury in patients susceptible to renal I/R after adequate clinical testing.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2319963"},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10903753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139973332","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

MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions. MTHFD2 介导的氧化还原稳态促进缺氧条件下的胃癌进展

IF 3.8 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-05-09 DOI: 10.1080/13510002.2024.2345455

Hai-Yu Mo, Ruo-Bing Wang, Meng-Yao Ma, Yi Zhang, Xin-Yu Li, Wang-Rong Wen, Yi Han, Tian Tian

{"title":"MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions.","authors":"Hai-Yu Mo, Ruo-Bing Wang, Meng-Yao Ma, Yi Zhang, Xin-Yu Li, Wang-Rong Wen, Yi Han, Tian Tian","doi":"10.1080/13510002.2024.2345455","DOIUrl":"10.1080/13510002.2024.2345455","url":null,"abstract":"Objectives: Cancer cells undergo metabolic reprogramming to adapt to high oxidative stress, but little is known about how metabolic remodeling enables gastric cancer cells to survive stress associated with aberrant reactive oxygen species (ROS) production. Here, we aimed to identify the key metabolic enzymes that protect gastric cancer (GC) cells from oxidative stress.Methods: ROS level was detected by DCFH-DA probes. Multiple cell biological studies were performed to identify the underlying mechanisms. Furthermore, cell-based xenograft and patient-derived xenograft (PDX) model were performed to evaluate the role of MTHFD2 in vivo.Results: We found that overexpression of MTHFD2, but not MTHFD1, is associated with reduced overall and disease-free survival in gastric cancer. In addition, MTHFD2 knockdown reduces the cellular NADPH/NADP+ ratio, colony formation and mitochondrial function, increases cellular ROS and cleaved PARP levels and induces in cell death under hypoxia, a hallmark of solid cancers and a common inducer of oxidative stress. Moreover, genetic or pharmacological inhibition of MTHFD2 reduces tumor burden in both tumor cell lines and patient-derived xenograft-based models.Discussion: our study highlights the crucial role of MTHFD2 in redox regulation and tumor progression, demonstrating the therapeutic potential of targeting MTHFD2.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2345455"},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11086033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140896275","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

Inhibition of SLC40A1 represses osteoblast formation via inducing iron accumulation and activating the PERK/ATF4/CHOP pathway mediated oxidative stress. 抑制SLC40A1通过诱导铁积累和激活PERK/ATF4/CHOP途径介导的氧化应激来抑制成骨细胞的形成。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-11-28 DOI: 10.1080/13510002.2024.2428147

Yu Fang, Wei Li, Chongyang Dong, Binli Gao, Wen Guo, Mingyu Li, Zhichao Jiao

{"title":"Inhibition of SLC40A1 represses osteoblast formation via inducing iron accumulation and activating the PERK/ATF4/CHOP pathway mediated oxidative stress.","authors":"Yu Fang, Wei Li, Chongyang Dong, Binli Gao, Wen Guo, Mingyu Li, Zhichao Jiao","doi":"10.1080/13510002.2024.2428147","DOIUrl":"10.1080/13510002.2024.2428147","url":null,"abstract":"Objective: This study aimed to investigate the effects of solute carrier family 40 member 1 (SLC40A1) on iron accumulation, oxidative stress and differentiation in osteoblasts and potential mechanisms.Methods: Mouse preosteoblastic MC3T3-E1 cells were transfected with the SLC40A1 overexpression vector (oeSLC40A1) and siRNA (siSLC40A1), then cell differentiation was induced via ascorbic acid and β-glycerophosphate. Besides, Ferrostatin-1 (ferroptosis inhibitor) and GSK2606414 (PERK inhibitor) were added with siSLC40A1.Results: Fe2+, malondialdehyde (MDA), and reactive oxygen species (ROS) were higher but reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio was lower after siSLC40A1 transfection, while reduced Fe2+ and ROS but elevated GSH/GSSG ratio was observed after oeSLC40A1 transfection. Alkaline phosphatase (ALP) staining, Alizarin Red S (ARS) staining, osteopontin (OPN) and bone morphogenetic protein 2 (BMP2) were lower after siSLC40A1 transfection but were greater after oeSLC40A1 transfection. Furthermore, SLC40A1 negatively regulated the PERK/ATF4/CHOP pathway. Further exploration revealed that Fe2+, MDA, ROS, and the PERK/ATF4/CHOP pathway were attenuated, while GSH/GSSG ratio, ALP staining, ARS staining, and OPN expression were increased after ferrostatin-1 treatment in the siSLC40A1-transfected cells. Similar trends were observed with respect to GSK2606414 treatment with siSLC40A1.Conclusion: SLC40A1 inhibition suppresses osteoblast formation by facilitating iron accumulation and activating the PERK/ATF4/CHOP pathway-mediated oxidative stress.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2428147"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11610352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751046","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

Palmitic acid and eicosapentaenoic acid supplementation in 3T3 adipocytes: impact on lipid storage and oxidative stress. 3T3脂肪细胞中棕榈酸和二十碳五烯酸的补充：对脂质储存和氧化应激的影响。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-11-28 DOI: 10.1080/13510002.2024.2430882

Edina Bakondi, Tobias Jung, Susanna Marg, Vanessa Schnell, Daniela Weber, Tim J Schulz, Tilman Grune, Annika Höhn

{"title":"Palmitic acid and eicosapentaenoic acid supplementation in 3T3 adipocytes: impact on lipid storage and oxidative stress.","authors":"Edina Bakondi, Tobias Jung, Susanna Marg, Vanessa Schnell, Daniela Weber, Tim J Schulz, Tilman Grune, Annika Höhn","doi":"10.1080/13510002.2024.2430882","DOIUrl":"10.1080/13510002.2024.2430882","url":null,"abstract":"Objectives: Obesity is a worldwide public health problem, predisposing individuals to serious cardiovascular and metabolic complications such as type 2 diabetes mellitus. White adipose tissue serves as an important regulator of energy balance, and its expansion in obesity can trigger inflammatory reactions and oxidative stress, which can also lead to insulin resistance. Adipocytes, with a key role in regulating metabolic homeostasis, respond to increased calorie intake and altered fatty acid composition with hypertrophy or hyperplasia. Of particular interest are saturated fatty acids such as palmitic acid and omega-3 polyunsaturated fatty acids such as eicosapentaenoic acid (EPA), which have differential effects on adipocyte function and inflammation.Methods: Using 3T3-L1 cells as a model for adipocytes, we evaluated the effects of PA and EPA on lipid accumulation, droplet size, and oxidative stress markers.Results: We were able to show that EPA supplementation in 3T3 adipocytes does not lead to excessive lipid accumulation, but rather reduces the size of lipid droplets and also induces redox changes due to the unsaturated nature of EPA.Discussion: These results emphasize the contrasting roles of PA and EPA and the importance of fatty acid composition in the regulation of adipocyte function.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2430882"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11610268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751162","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

Angelica keiskei water extract Mitigates Age-Associated Physiological Decline in Mice. 当归水提取物能缓解小鼠与年龄相关的生理机能衰退

IF 3.8 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-02-23 DOI: 10.1080/13510002.2024.2305036

Huan Liu, Gang Wei, Tongxing Wang, Yunlong Hou, Bin Hou, Xiaoyan Li, Chao Wang, Mingzhe Sun, Min Su, Zhifang Guo, Lu Wang, Ning Kang, Mengnan Li, Zhenhua Jia

{"title":"Angelica keiskei water extract Mitigates Age-Associated Physiological Decline in Mice.","authors":"Huan Liu, Gang Wei, Tongxing Wang, Yunlong Hou, Bin Hou, Xiaoyan Li, Chao Wang, Mingzhe Sun, Min Su, Zhifang Guo, Lu Wang, Ning Kang, Mengnan Li, Zhenhua Jia","doi":"10.1080/13510002.2024.2305036","DOIUrl":"10.1080/13510002.2024.2305036","url":null,"abstract":"Objective: Angelica keiskei is a medicinal and edible plant that has been reported to possess potent antioxidant properties in several in vitro models, but its effectiveness on naturally aging organisms is still lacking. This study explores the antioxidant and health-promoting effects of Angelica keiskei in naturally aging mice.Methods: We treated 48-week-old mice with Angelica keiskei water extract (AKWE) 30 days, and measured indicators related to aging and antioxidants. In addition, we conducted network pharmacology analysis, component-target molecular docking, real-time PCR, and MTS assays to investigate relevant factors.Results: The results indicated that administration of AKWE to mice led to decrease blood glucose levels, improve muscle fiber structure, muscle strength, gait stability, and increase levels of glutathione and superoxide dismutase in serum. Additionally, it decreased pigmentation of the heart tissues. Angelica keiskei combats oxidative stress by regulating multiple redox signaling pathways, and its ingredients Coumarin and Flavonoids have the potential to bind to SIRT3 and SIRT5.Conclusions: Our findings indicated the potential of Angelica keiskei as a safe and effective dietary supplement to combat aging and revealed the broad prospects of medicinal and edible plants for addressing aging and age-related chronic diseases.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2305036"},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139932664","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

Hyperglycemia-induced oxidative stress exacerbates mitochondrial apoptosis damage to cochlear stria vascularis pericytes via the ROS-mediated Bcl-2/CytC/AIF pathway. 高血糖诱导的氧化应激通过 ROS 介导的 Bcl-2/CytC/AIF 通路加剧了耳蜗血管纹周细胞线粒体凋亡损伤。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-08-02 DOI: 10.1080/13510002.2024.2382943

Tian-Feng Shi, Zan Zhou, Wen-Jun Jiang, Tian-Lan Huang, Jun-Qiang Si, Li Li

{"title":"Hyperglycemia-induced oxidative stress exacerbates mitochondrial apoptosis damage to cochlear stria vascularis pericytes via the ROS-mediated Bcl-2/CytC/AIF pathway.","authors":"Tian-Feng Shi, Zan Zhou, Wen-Jun Jiang, Tian-Lan Huang, Jun-Qiang Si, Li Li","doi":"10.1080/13510002.2024.2382943","DOIUrl":"10.1080/13510002.2024.2382943","url":null,"abstract":"Objectives: Diabetes is closely linked to hearing loss, yet the exact mechanisms remain unclear. Cochlear stria vascularis and pericytes (PCs) are crucial for hearing. This study investigates whether high glucose induces apoptosis in the cochlear stria vascularis and pericytes via elevated ROS levels due to oxidative stress, impacting hearing loss.Methods: We established a type II diabetes model in C57BL/6J mice and used auditory brainstem response (ABR), Evans blue staining, HE staining, immunohistochemistry, and immunofluorescence to observe changes in hearing, blood-labyrinth barrier (BLB) permeability, stria vascularis morphology, and apoptosis protein expression. Primary cultured stria vascularis pericytes were subjected to high glucose, and apoptosis levels were assessed using flow cytometry, Annexin V-FITC, Hoechst 33342 staining, Western blot, Mitosox, and JC-1 probes.Results: Diabetic mice showed decreased hearing thresholds, reduced stria vascularis density, increased oxidative stress, cell apoptosis, and decreased antioxidant levels. High glucose exposure increased apoptosis and ROS content in pericytes, while mitochondrial membrane potential decreased, with AIF and cytochrome C (CytC) released from mitochondria to the cytoplasm. Adding oxidative scavengers reduced AIF and CytC release, decreasing pericyte apoptosis.Discussion: Hyperglycemia may induce mitochondrial apoptosis of cochlear stria vascularis pericytes through oxidative stress.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2382943"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11299461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875818","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

Nobiletin protects against alcohol-induced mitochondrial dysfunction and liver injury by regulating the hepatic NRF1-TFAM signaling pathway. 金没药通过调节肝脏 NRF1-TFAM 信号通路，防止酒精诱导的线粒体功能障碍和肝损伤。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-09-02 DOI: 10.1080/13510002.2024.2395779

Dan Lu, Aiping Huang, Xiaoqing Tong, Xiaoyan Zhang, Songtao Li, Xiaolong Yu

{"title":"Nobiletin protects against alcohol-induced mitochondrial dysfunction and liver injury by regulating the hepatic NRF1-TFAM signaling pathway.","authors":"Dan Lu, Aiping Huang, Xiaoqing Tong, Xiaoyan Zhang, Songtao Li, Xiaolong Yu","doi":"10.1080/13510002.2024.2395779","DOIUrl":"10.1080/13510002.2024.2395779","url":null,"abstract":"Objectives: Alcohol and its metabolites, such as acetaldehyde, induced hepatic mitochondrial dysfunction play a pathological role in the development of alcohol-related liver disease (ALD).Methods: In this study, we investigated the potential of nobiletin (NOB), a polymethoxylated flavone, to counter alcohol-induced mitochondrial dysfunction and liver injury.Results: Our findings demonstrate that NOB administration markedly attenuated alcohol-induced hepatic steatosis, endoplasmic reticulum stress, inflammation, and tissue damage in mice. NOB reversed hepatic mitochondrial dysfunction and oxidative stress in both alcohol-fed mice and acetaldehyde-treated hepatocytes. Mechanistically, NOB restored the reduction of hepatic mitochondrial transcription factor A (TFAM) at both mRNA and protein levels. Notably, the protective effects of NOB against acetaldehyde-induced mitochondrial dysfunction and cell death were abolished in hepatocytes lacking Tfam. Furthermore, NOB administration reinstated the levels of hepatocellular NRF1, a key transcriptional regulator of TFAM, which were decreased by alcohol and acetaldehyde exposure. Consistent with these findings, hepatocyte-specific overexpression of Nrf1 protected against alcohol-induced hepatic Tfam reduction, mitochondrial dysfunction, oxidative stress, and liver injury.Conclusions: Our study elucidates the involvement of the NRF1-TFAM signaling pathway in the protective mechanism of NOB against chronic-plus-binge alcohol consumption-induced mitochondrial dysfunction and liver injury, suggesting NOB supplementation as a potential therapeutic strategy for ALD.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2395779"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142111441","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

Glutamine sustains energy metabolism and alleviates liver injury in burn sepsis by promoting the assembly of mitochondrial HSP60-HSP10 complex via SIRT4 dependent protein deacetylation. 谷氨酰胺通过 SIRT4 依赖性蛋白去乙酰化促进线粒体 HSP60-HSP10 复合物的组装，从而维持能量代谢并减轻烧伤败血症对肝脏的损伤。

IF 3.8 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-02-08 DOI: 10.1080/13510002.2024.2312320

Yongjun Yang, Qian Chen, Shijun Fan, Yongling Lu, Qianyin Huang, Xin Liu, Xi Peng

{"title":"Glutamine sustains energy metabolism and alleviates liver injury in burn sepsis by promoting the assembly of mitochondrial HSP60-HSP10 complex via SIRT4 dependent protein deacetylation.","authors":"Yongjun Yang, Qian Chen, Shijun Fan, Yongling Lu, Qianyin Huang, Xin Liu, Xi Peng","doi":"10.1080/13510002.2024.2312320","DOIUrl":"10.1080/13510002.2024.2312320","url":null,"abstract":"Burns and burn sepsis, characterized by persistent and profound hypercatabolism, cause energy metabolism dysfunction that worsens organ injury and systemic disorders. Glutamine (Gln) is a key nutrient that remarkably replenishes energy metabolism in burn and sepsis patients, but its exact roles beyond substrate supply is unclear. In this study, we demonstrated that Gln alleviated liver injury by sustaining energy supply and restoring redox balance. Meanwhile, Gln also rescued the dysfunctional mitochondrial electron transport chain (ETC) complexes, improved ATP production, reduced oxidative stress, and protected hepatocytes from burn sepsis injury. Mechanistically, we revealed that Gln could activate SIRT4 by upregulating its protein synthesis and increasing the level of Nicotinamide adenine dinucleotide (NAD+), a co-enzyme that sustains the activity of SIRT4. This, in turn, reduced the acetylation of shock protein (HSP) 60 to facilitate the assembly of the HSP60-HSP10 complex, which maintains the activity of ETC complex II and III and thus sustain ATP generation and reduce reactive oxygen species release. Overall, our study uncovers a previously unknown pharmacological mechanism involving the regulation of HSP60-HSP10 assembly by which Gln recovers mitochondrial complex activity, sustains cellular energy metabolism and exerts a hepato-protective role in burn sepsis.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2312320"},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139703239","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

Mitochondrial dysfunction induced in human hepatic HepG2 cells exposed to the fungicide kresoxim-methyl and to a mixture kresoxim-methyl/boscalid. 暴露于杀真菌剂克瑞肟菌甲和克瑞肟菌甲/啶酰菌胺混合物的人类肝脏 HepG2 细胞诱发线粒体功能障碍。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1080/13510002.2024.2424677

Yasmine Vandensande, Mélina Carbone, Barbara Mathieu, Bernard Gallez

{"title":"Mitochondrial dysfunction induced in human hepatic HepG2 cells exposed to the fungicide kresoxim-methyl and to a mixture kresoxim-methyl/boscalid.","authors":"Yasmine Vandensande, Mélina Carbone, Barbara Mathieu, Bernard Gallez","doi":"10.1080/13510002.2024.2424677","DOIUrl":"10.1080/13510002.2024.2424677","url":null,"abstract":"The fungicides strobilurins and succinate dehydrogenase inhibitors (SDHIs) are blockers of the electron transport chain (ETC) in fungi. Here, we show that the exposure for 24 h to kresoxym-methyl, a fungicide from the class of strobilurins, alters the mitochondrial respiration in human HepG2 hepatocytes. In addition, we demonstrate an increase in production of mitochondrial superoxide radical anion, a reduction in ATP level, a decrease in the ratio reduced/oxidized glutathione and a decrease in cell viability (assessed by the LDH assay, Presto Blue assay, and Crystal Violet assay). As kresoxym-methyl is associated to boscalid (SDHI) in commercial formulations, we analyzed a potential exacerbation of the induced mitochondrial dysfunction for this combination. For the highest dose at which kresoxym-methyl (5 µM) and boscalid (0.5 µM) did not induce changes in mitochondrial function when used separately, in contrast, when both fungicides were used in combination at the same concentration, we observed a significant alteration of the mitochondrial function of hepatocytes: there was a decrease in oxygen consumption rate, in the ATP level. In addition, the level of mitochondrial superoxide radical anion was increased leading to a decrease in the ratio reduced/oxidized glutathione, and an increase in viability.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2424677"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11565682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142626717","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

Jaceosidin induces apoptosis and inhibits migration in AGS gastric cancer cells by regulating ROS-mediated signaling pathways. 栀子苷通过调节 ROS 介导的信号通路诱导 AGS 胃癌细胞凋亡并抑制其迁移。

IF 3.8 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-02-06 DOI: 10.1080/13510002.2024.2313366

Jian Liu, Shu-Mei Li, Yan-Jun Tang, Jing-Long Cao, Wen-Shuang Hou, An-Qi Wang, Chang Wang, Cheng-Hao Jin

{"title":"Jaceosidin induces apoptosis and inhibits migration in AGS gastric cancer cells by regulating ROS-mediated signaling pathways.","authors":"Jian Liu, Shu-Mei Li, Yan-Jun Tang, Jing-Long Cao, Wen-Shuang Hou, An-Qi Wang, Chang Wang, Cheng-Hao Jin","doi":"10.1080/13510002.2024.2313366","DOIUrl":"10.1080/13510002.2024.2313366","url":null,"abstract":"Jaceosidin (JAC) is a natural flavonoid with anti-oxidant and other pharmacological activities; however, its anti-cancer mechanism remains unclear. We investigated the mechanism of action of JAC in gastric cancer cells. Cytotoxicity and apoptosis assays showed that JAC effectively killed multiple gastric cancer cells and induced apoptosis in human gastric adenocarcinoma AGS cells via the mitochondrial pathway. Network pharmacological analysis suggested that its activity was linked to reactive oxygen species (ROS), AKT, and MAPK signaling pathways. Furthermore, JAC accumulated ROS to up-regulate p-JNK, p-p38, and IκB-α protein expressions and down-regulate the p-ERK, p-STAT3, and NF-κB protein expressions. Cell cycle assay results showed that JAC accumulated ROS to up-regulate p21 and p27 protein expressions and down-regulate p-AKT, CDK2, CDK4, CDK6, Cyclin D1, and Cyclin E protein expressions to induce G0/G1 phase arrest. Cell migration assay results showed JAC accumulated ROS to down-regulate Wnt-3a, p-GSK-3β, N-cadherin, and β-catenin protein expressions and up-regulate E-cadherin protein expression to inhibit migration. Furthermore, N-acetyl cysteine pre-treatment prevented the change of these protein expressions. In summary, JAC induced apoptosis and G0/G1 phase arrest and inhibited migration through ROS-mediated signaling pathways in AGS cells.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2313366"},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139692840","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