Redox Report最新文献_第3页

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

Skeletal muscle cystathionine γ-lyase deficiency promotes obesity and insulin resistance and results in hyperglycemia and skeletal muscle injury upon HFD in mice. 小鼠骨骼肌胱硫醚γ-赖氨酸酶缺乏症会促进肥胖和胰岛素抵抗，并导致高血糖和骨骼肌损伤。

IF 3.8 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-05-08 DOI: 10.1080/13510002.2024.2347139

Jiani Lu, Zhengshan Tang, Miaomiao Xu, Jianqiang Lu, Fengmei Wang, Xin Ni, Changnan Wang, Bo Yu

{"title":"Skeletal muscle cystathionine γ-lyase deficiency promotes obesity and insulin resistance and results in hyperglycemia and skeletal muscle injury upon HFD in mice.","authors":"Jiani Lu, Zhengshan Tang, Miaomiao Xu, Jianqiang Lu, Fengmei Wang, Xin Ni, Changnan Wang, Bo Yu","doi":"10.1080/13510002.2024.2347139","DOIUrl":"10.1080/13510002.2024.2347139","url":null,"abstract":"Objectives: The objective of this study was to investigate whether skeletal muscle cystathionine γ-lyase (CTH) contributes to high-fat diet (HFD)-induced metabolic disorders using skeletal muscle Cth knockout (CthΔskm) mice.Methods: The CthΔskm mice and littermate Cth-floxed (Cthf/f) mice were fed with either HFD or chow diet for 13 weeks. Metabolomics and transcriptome analysis were used to assess the impact of CTH deficiency in skeletal muscle.Results: Metabolomics coupled with transcriptome showed that CthΔskm mice displayed impaired energy metabolism and some signaling pathways linked to insulin resistance (IR) in skeletal muscle although the mice had normal insulin sensitivity. HFD led to reduced CTH expression and impaired energy metabolism in skeletal muscle in Cthf/f mice. CTH deficiency and HFD had some common pathways enriched in the aspects of amino acid metabolism, carbon metabolism, and fatty acid metabolism. CthΔskm+HFD mice exhibited increased body weight gain, fasting blood glucose, plasma insulin, and IR, and reduced glucose transporter 4 and CD36 expression in skeletal muscle compared to Cthf/f+HFD mice. Impaired mitochondria and irregular arrangement in myofilament occurred in CthΔskm+HFD mice. Omics analysis showed differential pathways enriched between CthΔskm mice and Cthf/f mice upon HFD. More severity in impaired energy metabolism, reduced AMPK signaling, and increased oxidative stress and ferroptosis occurred in CthΔskm+HFD mice compared to Cthf/f+HFD mice.Discussion: Our results indicate that skeletal muscle CTH expression dysregulation contributes to metabolism disorders upon HFD.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2347139"},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140892536","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

Characterization of naphthoquinones as inhibitors of glutathione reductase and inducers of intracellular oxidative stress.

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-12-02 DOI: 10.1080/13510002.2024.2432830

Xiaowan Chen, Yan Ma, Ziming Yang, Dingjie Shen, Xia Li, Maowei Ni, Xiaoling Xu, Wei Chen

{"title":"Characterization of naphthoquinones as inhibitors of glutathione reductase and inducers of intracellular oxidative stress.","authors":"Xiaowan Chen, Yan Ma, Ziming Yang, Dingjie Shen, Xia Li, Maowei Ni, Xiaoling Xu, Wei Chen","doi":"10.1080/13510002.2024.2432830","DOIUrl":"10.1080/13510002.2024.2432830","url":null,"abstract":"Glutathione reductase (GR), one of the most important antioxidant enzymes in maintaining intracellular redox homeostasis, has become a novel target to suppress cancer cell growth and metastasis. In this work, we evaluated a series of naphthoquinones (NQs) as potential GR inhibitors and elucidated the mechanism of inhibition. NQ-6, one of the most potent compounds among this series, inhibited GR in vitro and in vivo and was identified as a competitive and irreversible inhibitor. The Ki and kinact values of NQ-6 were determined to be 17.30 ± 3.63 μM and 0.0136 ± 0.0005 min-1, respectively. The tandem mass spectrometric analysis revealed that the two substrate binding sites Cys61 and Cys66 of yeast GR were modified simultaneously through arylation or only Cys66 was covalently modified by NQ-6. Intracellular reactive oxygen species, collapsing of mitochondrial membrane potential and protein S-glutathionylation elevation were induced by NQ-6. NQs can be valuable compounds in GR inhibition and oxidative stress-related research.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2432830"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142771802","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

Sigma-1 receptor exerts protective effects on ameliorating nephrolithiasis by modulating endoplasmic reticulum-mitochondrion association and inhibiting endoplasmic reticulum stress-induced apoptosis in renal tubular epithelial cells. Sigma-1 受体通过调节肾小管上皮细胞的内质网-线粒体结合和抑制内质网应激诱导的细胞凋亡，对改善肾炎具有保护作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-08-13 DOI: 10.1080/13510002.2024.2391139

Hu Ke, Xiaozhe Su, Caitao Dong, Ziqi He, Qianlin Song, Chao Song, Jiawei Zhou, Wenbiao Liao, Chuan Wang, Sixing Yang, Yunhe Xiong

{"title":"Sigma-1 receptor exerts protective effects on ameliorating nephrolithiasis by modulating endoplasmic reticulum-mitochondrion association and inhibiting endoplasmic reticulum stress-induced apoptosis in renal tubular epithelial cells.","authors":"Hu Ke, Xiaozhe Su, Caitao Dong, Ziqi He, Qianlin Song, Chao Song, Jiawei Zhou, Wenbiao Liao, Chuan Wang, Sixing Yang, Yunhe Xiong","doi":"10.1080/13510002.2024.2391139","DOIUrl":"10.1080/13510002.2024.2391139","url":null,"abstract":"Oxalate-induced damage to renal tubular epithelial cells (RTECs) is an essential factor in the incident kidney stone, but the specific mechanism is unclear. Recent research has pinpointed interacting areas within the endoplasmic reticulum and mitochondria, called mitochondria-associated membranes (MAMs). These studies have linked endoplasmic reticulum stress (ERS) and oxidative imbalance to kidney disease development. The sigma-1 receptor (S1R), a specific protein found in MAMs, is involved in various physiological processes, but its role in oxalate-induced kidney stone formation remains unclear. In this study, we established cellular and rat models of oxalate-induced kidney stone formation to elucidate the S1R's effects against ERS and apoptosis and its mechanism in oxalate-induced RTEC injury. We found that oxalate downregulated S1R expression in RTECs and escalated oxidative stress and ERS, culminating in increased apoptosis. The S1R agonist dimemorfan up-regulated S1R expression and mitigated ERS and oxidative stress, thereby reducing apoptosis. This protective effect was mediated through S1R inhibition of the CHOP pathway. Animal experiments demonstrated that S1R's activation attenuated oxalate-induced kidney injury and alleviated kidney stone formation. This is the first study to establish the connection between S1R and kidney stones, suggesting S1R's protective role in inhibiting ERS-mediated apoptosis to ameliorate kidney stone formation.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2391139"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11328816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141976509","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

Assessment of renal pathophysiological processes and protective effect of quercetin on contrast-induced acute kidney injury in type 1 diabetic mice using diffusion tensor imaging. 利用弥散张量成像评估 1 型糖尿病小鼠的肾脏病理生理过程以及槲皮素对造影剂诱发的急性肾损伤的保护作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-09-16 DOI: 10.1080/13510002.2024.2398380

Ziqian Wu, Jingyi Hu, Yanfei Li, Xiang Yao, Siyu Ouyang, Ke Ren

{"title":"Assessment of renal pathophysiological processes and protective effect of quercetin on contrast-induced acute kidney injury in type 1 diabetic mice using diffusion tensor imaging.","authors":"Ziqian Wu, Jingyi Hu, Yanfei Li, Xiang Yao, Siyu Ouyang, Ke Ren","doi":"10.1080/13510002.2024.2398380","DOIUrl":"https://doi.org/10.1080/13510002.2024.2398380","url":null,"abstract":"Purpose: To investigate the renal pathophysiological processes and protective effect of quercetin on contrast-induced acute kidney injury (CI-AKI) in mice with type 1 diabetic mellitus(DM) using diffusion tensor imaging(DTI).Methods: Mice with DM were divided into two groups. In the diabetic + contrast medium(DCA) group, the changes of the mice kidneys were monitored at 1, 24, 48, and 72 h after the injection of iodixanol(4gI/kg). The mice in the diabetic + contrast medium + quercetin(DCA + QE) group were orally given different concentrations of quercetin for seven days before injection of iodixanol. In vitro experiments, renal tubular epithelial (HK-2) cells exposed to high glucose conditions were treated with various quercetin concentrations before treatment with iodixanol(250 mgI/mL).Results: DTI-derived mean diffusivity(MD) and fractional anisotropy(FA) values can be used to evaluate CI-AKI effectively. Quercetin significantly increased the expression of Sirt 1 and reduced oxidative stress by increasing Nrf 2/HO-1/SOD1. The antiapoptotic effect of quercetin on CI-AKI was revealed by decreasing proteins level and by reducing the number of apoptosis-positive cells. In addition, flow cytometry indicated quercetin-mediated inhibition of M1 macrophage polarization in the CI-AKI.Conclusions: DTI will be an effective noninvasive tool in diagnosing CI-AKI. Quercetin attenuates CI-AKI on the basis of DM through anti-oxidative stress, apoptosis, and inflammation.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2398380"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11407404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142294175","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