DESALINATION
·
2014
·
IF 3.96
Yaojie Li,Lifen Liu,Jiadong Liu,Fenglin Yang,Nanqi Ren
To increase effluent quality and membrane flux , membrane bioreactor was integrated with microbial fuel cell (MBR/MFC), in which functional cathode membranes could enable fouling reduction and even electro-catalytic pollutant degradation using the bio-generated electricity. Modifying stainless steel mesh (SSM) with only polypyrrole (PPy) or cheap ARS (Alizarin Red's) or expensive AQS (9,10-anthraquinone-2-sulfonic acid) doped PPy film, helped obtain high ORR (oxygen reduction reaction) activity and higher power output in the integrated MBR/MFC system. The ARS and PPy modified cathode membranes, could not only increase the degradation of (MB) methylene blue (> 90%, 1 h), but also enable higher antifouling property in filtrations. Most importantly, replacing the blank SSM, the use of PPy/AQS, PPy/ARS and PPy modified SSM, increased power density 31.37, 27.06 and 23.7 times respectively in the integrated MBR/MFC system. The new system has great application potential and economic feasibility in effective removal of COD and NH 4 + -N nutrients, has better effluent qualities and has higher energy recovery.
研究领域:
环境科学
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生物技术
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材料科学
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DOI
高影响因子
JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
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2023
·Vol. 104
·期 1
·479-487
·
IF 4.1
Zhihai Liu,Ce Ma,Hongwei Gao,Xiaoli Huang,Yaru Zhang,Congmin Liu,Ranran Hou,Qidi Zhang,Qiu Li
BACKGROUND Obesity, a global chronic disease, has been recognized as a severe risk to health. In our study, a novel polysaccharide named ARS was isolated and purified from aerial part of salviae miltiorrhizae radix . Our aim is to investigate the weight-reducing effect of a polysaccharide from salviae miltiorrhizae radix on mice fed a high-fat diet. RESULTS The novel polysaccharide ARS mainly consisted of glucose and galactose with a molar ratio of 0.59:1.00. We found that treatment with ARS could inhibit weight gain of mice fed a high-fat diet via modulating the intestinal bacteria. Moreover, we surveyed its mechanism in mice, and the gut microbiota sequencing results demonstrated that ARS can reverse or resist high-fat-diet-induced significant weight gain or obesity by increasing the diversity of gut microbiota and optimizing the ratio of Firmicutes to Bacteroidetes. Phylum and species analysis of gut microbiota demonstrated that obesity caused by a high-fat diet was accompanied by significant changes in the microbial communities, but ARS could reverse the disturbance of gut microbiota induced by the high-fat diet to maintain homeostasis. CONCLUSION Overall, our findings suggested a new function of ARS in regulating gut microbiota, which provides a theoretical basis for the development of high-quality ARS functional foods and the application of dietary supplements. © 2023 Society of Chemical Industry.
研究领域:
营养学
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微生物学
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药理学
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DOI
PubMed
高影响因子
MICROBIOLOGICAL RESEARCH
·
2024
·
IF 6.1
Ruixiang Yang,Thiruselvam Viswanatham,Shuangqin Huang,Yuanping Li,Yanshuang Yu,Jinlin Zhang,Jian Chen,Martin Herzberg,Renwei Feng,Barry P. Rosen,Christopher Rensing
Antimony is pervasive environmental toxic substance, and numerous genes encoding mechanisms to resist, transform and extrude the toxic metalloid antimony have been discovered in various microorganisms. Here we identified a major facilitator superfamily (MFS) transporter, AntB, on the chromosome of the arsenite-oxidizing bacterium Ensifer adhaerens E-60 that confers resistance to Sb(III) and Sb(V). The antB gene is adjacent to gene encoding a LysR family transcriptional regulator termed LysR ars , which is an As(III)/Sb(III)-responsive transcriptional repressor that is predicted to control expression of antB . Similar antB and lysR ars genes are found in related arsenic-resistant bacteria, especially strains of Ensifer adhaerens , and the lysR ars gene adjacent to antB encodes a member of a divergent subgroup of putative LysR-type regulators. Closely related AntB and LysR ars orthologs contain three conserved cysteine residues, which are Cys17, Cys99, and Cys350 in AntB and Cys81, Cys289 and Cys294 in LysR ars , respectively. Expression of antB is induced by As(III), Sb(III), Sb(V) and Rox(III) (4-hydroxy-3-nitrophenyl arsenite). Heterologous expression of antB in E. coli AW3110 (Δ ars ) conferred resistance to Sb(III) and Sb(V) and reduced the intracellular concentration of Sb(III). The discovery of the Sb(III) efflux transporter AntB enriches our knowledge of the role of the efflux transporter in the antimony biogeochemical cycle .
研究领域:
微生物学
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环境科学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2024
·
IF 5.9
Siyu Lu,Yiming Zhou,Mincong Liu,Lijun Gong,Li Liu,Zhigui Duan,Keke Chen,Frank J. Gonzalez,Fang Wei,Rong Xiang,Guolin Li
Aims: Redox signaling plays a key role in skeletal muscle remodeling induced by exercise and prolonged inactivity, but it is unclear which oxidant triggers myofiber hypertrophy due to the lack of strategies to precisely regulate individual oxidants in vivo. In this study, we used tetrathiomolybdate (TM) to dissociate the link between superoxide (O2•−) and hydrogen peroxide and thereby to specifically explore the role of O2•− in muscle hypertrophy in C2C12 cells and mice.Results: TM can linearly regulate intracellular O2•− levels by inhibition of superoxide dismutase 1 (SOD1). A 70% increase in O2•− levels in C2C12 myoblast cells and mice is necessary and sufficient for triggering hypertrophy of differentiated myotubes and can enhance exercise performance by more than 50% in mice. SOD1 knockout blocks TM-induced O2•− increments and thereby prevents hypertrophy, whereas SOD1 restoration rescues all these effects. Scavenging O2•− with antioxidants abolishes TM-induced hypertrophy and the enhancement of exercise performance, whereas the restoration of O2•− levels with a O2•− generator promotes muscle hypertrophy independent of SOD1 activity.Innovation and Conclusion: These findings suggest that O2•− is an endogenous initiator of myofiber hypertrophy and that TM may be used to treat muscle wasting diseases. Our work not only suggests a novel druggable mechanism to increase muscle mass but also provides a tool for precisely regulating O2•− levels in vivo.
研究领域:
生理学
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药理学
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运动科学
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产品关联
DOI
PubMed
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2024
·
IF 5.9
Yecheng Wang,Caiyun Huang,Xiaoying Wang,Rong Cheng,Xue Li,Jiahao Wang,Lu Zhang,Fuhao Li,Hao Wang,Xinyu Li,Yi Li,Yiqing Xia,Jian Cheng,Xiaofan Pan,Jia Jia,Guo-dong Xiao
Aims: Succinate, a metabolite in the tricarboxylic acid cycle, is increasingly recognized to play essential roles in inflammation by functioning either as an intracellular or extracellular signaling molecule. However, the role and mechanisms of succinate in inflammation remain elusive. Here, we investigated the mechanism underlying the effects of succinate on neuroinflammation in intracerebral hemorrhage (ICH) models. Results: We unexpectedly found that succinate robustly inhibited neuroinflammation and conferred protection following ICH. Mechanistically, oxidation of succinate by succinate dehydrogenase (SDH) drove reverse electron transport (RET) at mitochondrial complex I, leading to mitochondrial superoxide production in microglia. Complex I-derived superoxide, in turn, activated uncoupling protein 2 (UCP2). By using mice with specific deletion of UCP2 in microglia/macrophage, we showed that UCP2 was needed for succinate to inhibit neuroinflammation, confer protection, and activate downstream AMP-activated protein kinase (AMPK) following ICH. Moreover, knockdown of SDH, complex I or AMPK abolished the therapeutic effects of succinate following ICH. Innovation and Conclusion: We provide evidence that driving complex I RET to activate UCP2 is a novel mechanism of succinate intracellular signaling and a mechanism underlying the inhibition of neuroinflammation by succinate. Key words: succinate; uncoupling protein 2; microglia; neuroinflammation; intracerebral hemorrhage
研究领域:
神经科学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2025
·
IF 6.1
Xian-Dong Li,Yue-Xin Ning,Yi-Feng Pei,Jing-Yuan Niu,Jian Luo,Yi-Na Zhang,Zi-Ai Zhao,Xiao-Wen Hou,Qian-Kun Zhao,Tian-Ce Xu,Hui-Sheng Chen
Aims: Cathodal transcranial direct current stimulation (C-tDCS), a noninvasive physical therapy, has potential neuroprotective effects in acute ischemic stroke. However, the rational timing of its application and the underlying mechanisms remain inadequately understood. This study aims to investigate its neuroprotective effects and the involved mechanisms.Results: Our in vivo results indicated that C-tDCS applied during the reperfusion phase but not during the ischemic phase significantly improved neurological outcomes, reduced infarct volume, and mitigated histopathological damage in middle cerebral artery occlusion/reperfusion rats. C-tDCS during the reperfusion phase suppressed ferroptosis, activated nuclear factor erythroid 2-related factor 2 (Nrf2), and inhibited mitophagy. In vitro, the ferroptosis inducer RSL3 negated the protective effects of cathodal direct current stimulation on HT22 neuronal cells subjected to oxygen-glucose deprivation/reoxygenation injury. Furthermore, the Nrf2 inhibitor ML385 and the mitophagy activator FCCP reversed the inhibitory effects of C-tDCS on ferroptosis, with FCCP also affecting Nrf2 activation by C-tDCS.Innovation and Conclusions: These results demonstrate that C-tDCS during reperfusion attenuates cerebral ischemia-reperfusion injury by coordinating mitophagy inhibition and Nrf2 activation to counteract ferroptosis, which provides new evidence for its potential translational clinical applications. Antioxid. Redox Signal. 00, 000–000.
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产品关联
DOI
PubMed
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2025
·
IF 6.1
Wenhui Yan,Xin Cui,Tingli Guo,Na Liu,Zhuanzhuan Wang,Yuzhuo Sun,Yuanrui Shang,Jieyun Liu,Yuanyuan Zhu,Yangyang Zhang,Lina Chen
Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent hepatic disorder worldwide. Arachidonic acid 15-lipoxygenase (ALOX15), an enzyme catalyzing the peroxidation of polyunsaturated fatty acids, plays a crucial role in various diseases. Here, we sought to investigate the involvement of ALOX15 in MASLD.Results: In this study, we observed upregulation of ALOX15 in the liver of high-fat diet (HFD)- and streptozotocin (STZ)-induced mice. Metabolomic analysis revealed elevated levels of ALOX15 metabolites, 12(S)-hydroperoxyeicosatetraenoic acid and 15(S)-hydroperoxyeicosatetraenoic acid. Transcriptomic analysis showed that the increased fatty acid uptake regulated by the PPARγ/CD36 pathway predominated in lipid accumulation. To elucidate the mechanism underlying ALOX15-induced lipid accumulation, HepG2 cells were transfected with a lentivirus expressing ALOX15 or small interfering RNA targeting ALOX15 and exposed to palmitic acid (PA). Both ALOX15 overexpression and PA exposure led to increased intracellular free fatty acid and triglyceride, resulting in lipotoxicity. ALOX15 overexpression aggravated the effect of PA, while the knockdown of ALOX15 attenuated PA-induced lipotoxicity. Moreover, the treatment with PPARγ antagonist GW9662 or CD36 inhibitor sulfosuccinimidyl oleate sodium effectively reduced lipid accumulation and lipotoxicity resulting from ALOX15 overexpression and PA exposure, indicating the involvement of the PPARγ/CD36 pathway in ALOX15-mediated lipid accumulation. Furthermore, liraglutide, a widely used glucagon-like peptide 1 receptor (GLP-1R) agonist (GLP-1RA), improved hepatic lipid accumulation in HFD/STZ-induced mice by suppressing the ALOX15/PPARγ/CD36 pathway.Innovation and Conclusion: Our study underscores the potential of ALOX15 as an emerging therapeutic target for MASLD. In addition, the GLP-1RA may confer hepatoprotection by regulating ALOX15, enhancing our comprehension of the mechanisms underpinning their protection on MASLD. Antioxid. Redox Signal. 00, 000–000.
研究领域:
肝病学
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内分泌学
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分子生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2009
·
IF 6.19
Achuthan Raghavamenon,Mahdi Garelnabi,Sainath Babu,Alex Aldrich,Dmitry Litvinov,Sampath Parthasarathy
The decomposition of peroxidized lipids of low-density lipoprotein (LDL) has been suggested to be involved in atherosclerosis. In this study, an in vitro system with 13-hydroperoxylinoleic acid (13-HPODE) was used to determine the effects of antioxidants on its decomposition. Decomposition of 13-HPODE was not affected by α-tocopherol, several other antioxidants, or antioxidant enzymes. Moreover, the inclusion of α-tocopherol during the decomposition of 13-HPODE resulted in an accumulation of aldehydes. Further oxidation of aldehydes to carboxylic acids by a number of oxidases was prevented by α-tocopherol. Conversely, the formation of carboxylic acids may be conducive to plaque stabilization via immunomodulation, rapid degradation, and by calcium sequestration. Thus, the inhibition of formation of carboxylic acids could be a serious deleterious effect of antioxidant treatment. In contrast, α-keto acids, like pyruvic acid, promoted the conversion of 13-HPODE to 13-hydroxylinoleic acid (13-HODE) by readily undergoing decarboxylation into acetate. These observations suggest that agents that promote the reduction of lipid peroxides into lipid hydroxides could be far more effective in treating cardiovascular diseases as opposed α-tocopherol–like antioxidants that could affect additional steps in the oxidation cascade. Antioxid. Redox Signal. 11, 1237–1248.
研究领域:
生物化学
·
心血管疾病研究
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氧化应激
·
药理学
·
分子生物学
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DOI
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2019
·Vol. 30
·期 12
·1503-1520
·
IF 5.828
Tingting Chen,Yichen Guo,Jinjun Shan,Jiarui Zhang,Xu Shen,Jun Guo,Xiaoguang Margaret Liu
Aims: Pyroptotic cells are characterized by plasma swelling, membrane blebbing, and disintegration of the cell membrane mediated by spectrin-based membrane skeleton and intercellular competitive tension activities. The spectrin-based membrane skeleton is involved in membrane organization through the regulation of intercellular tension. Using genetically encoded tension sensors to attain noninvasive force measurements in structural proteins, we investigated how cytoskeletal structural tension influences changes in plasma morphology during pyroptosis and the regulatory mechanism of cytoskeletal structural tension that underpins pyroptosis.Results: The results indicate that increasing spectrin tension is caused by osmotic swelling. Hightened tension of spectrin was closely associated with the shrink tension transmitted synergistically by microfilaments (MFs) and microtubules (MTs). However, the increment of spectrin tension in pyroptotic cells was controlled antagonistically by MF and MT forces. Different from MF tension, outward MT forces participated in the formation of membrane blebs. Spectrin tension caused by inward MF forces resisted pyroptosis swelling. Stabilization of MF and MT structure had little influence on intracellular tension and pyroptosis deformation. Pyroptosis-induced cytoskeletal structural tension was highly dependent on calcium signaling and reactive oxygen species generation. Blocking of membrane pores, nonselective ion flux, or elimination of caspase-1 cleavage resulted in the remission of structural forces associated with pyroptosis failure.Innovation and Conclusions: The data suggest that subcellular tension, in terms of magnitude and vector, is integral to pyroptosis through the mediation of swelling and blebbing and the elimination of structural tension, especially MT forces, may result in pyroptosis inhibition.
研究领域:
细胞生物学
·
分子生物学
·
免疫学
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产品关联
DOI
PubMed
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2023
·
IF 6.6
Dr. Jiedong Zhou,Dr. Jinjin Hao,Dr. Zuoquan Zhong,Dr. Juntao Yang,Dr. Tingting Lv,Mr. Bingjie Zhao,Dr. Hui Lin,Dr. Jufang Chi,Dr. Hangyuan Guo
Aims: The relationship between gut microbiota and cardiovascular system has been increasingly clarified. Fecal microbiota transplantation (FMT), used to improve gut microbiota, has been applied clinically for disease treatment and has great potential in combatting doxorubicin (DOX)-induced cardiotoxicity. However, the application of FMT in the cardiovascular field and its molecular mechanisms are poorly understood.
Results: During DOX-induced stress, FMT alters the gut microbiota and serum metabolites, leading to a reduction in cardiac injury. Correlation analysis indicated a close association between serum metabolite Indole-3-propionic acid (IPA) and cardiac function. FMT and IPA achieves this by facilitating the translocation of Nfe2l2 (Nrf2) from the cytoplasm to the nucleus, thereby activating the expression of antioxidant molecules, reducing ROS production, and inhibiting excessive mitochondrial fission. Consequently, mitochondrial function is preserved, leading to the mitigation of cardiac injury under DOX-induced stress.
Innovation: FMT has the ability to modify the composition of the gut microbiota, providing not only protection to the intestinal mucosa but also influencing the generation of serum metabolites and regulating the Nrf2 gene to modulate the balance of cardiac mitochondrial fission and fusion. This study comprehensively demonstrates the efficacy of FMT in countering DOX-induced myocardial damage and elucidates the pathways linking the microbiota and the heart.
Conclusion: FMT alters the gut microbiota and serum metabolites of recipient mice, promoting nuclear translocation of Nrf2 and subsequent activation of downstream antioxidant molecule expression, while inhibiting excessive mitochondrial fission to preserve cardiac integrity. Correlation analysis highlights IPA as a key contributor among differentially regulated metabolites.
研究领域:
心脏病学
·
药理学
·
微生物学
·
分子生物学
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产品关联
DOI
PubMed
高影响因子
Bioactive Materials
·
2022
·
IF 16.874
Haiwei Liang,Yanxiao Ao,Wenjing Li,Kaini Liang,Baixue Tang,Junyang Li,Jianwei Wang,Xiaoyu Zhu,Yanan Du
Hematopoietic syndrome of acute radiation syndrome (h-ARS) is an acute illness resulted from the damage of bone marrow (BM) microenvironment after exposure to radiation. Currently, the clinical management of h-ARS is limited to medication-assisted treatment, while there is still no specific therapy for the hematopoietic injury from high-dose radiation exposure. Our study aimed to assemble biomimetic three-dimensional (3D) BM microniches by co-culture of hematopoietic stem and progenitor cells (HSPCs) and mesenchymal stem cells (MSCs) in porous, injectable and viscoelastic microscaffolds in vitro . The biodegradable BM microniches were then transplanted in vivo into the BM cavity for the treatment of h-ARS. We demonstrated that the maintenance of HSPCs was prolonged by co-culture with MSCs in the porous 3D microscaffolds with 84 μm in pore diameter and 11.2 kPa in Young's modulus compared with 2D co-culture system. Besides, the minimal effective dose and therapeutic effects of the BM microniches were investigated on a murine model of h-ARS, which showed that the intramedullary cavity-injected BM microniches could adequately promote hematopoietic reconstitution and mitigate death from acute lethal radiation with a dose as low as 1000 HSPCs. Furthermore, the mRNA expression of Notch1 and its downstream target gene Hes1 of HSPCs were increased when co-cultured with MSCs, while the Jagged1 expression of the co-cultured MSCs was upregulated, indicating the significance of Notch signaling pathway in maintenance of HSPCs. Collectively, our findings provide evidence that biomimetic and injectable 3D BM microniches could maintain HSPCs, promote hematopoiesis regeneration and alleviate post-radiation injury, which provides a promising approach to renovate conventional HSPCs transplantation for clinical treatment of blood and immune disorders.
研究领域:
干细胞研究
·
再生医学
·
辐射生物学
·
组织工程
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DOI
PubMed
高影响因子
BIOSENSORS & BIOELECTRONICS
·
2016
·
IF 7.476
Bing Zhang,Chuanmin Ding
The sensitive determination of carcino embryonie antigen (CEA)-a set of highly related glycoproteins involved in cell adhesion-is beneficial to the early diagnosis of colorectal cancer. In this study, a novel displacement-type amperometric immunosensing platform, based on the fact that glucose and Alizarin Red S (ARS) compete for phenylboronic acid bindng sites, was projected for sensitive detection of tumour marker (CEA, used as a model) on a PAMAM dendrimer-encapsulated nanogold (PAMAM-Au)-functionlized sensing interface. Firstly, 4 − mercaptophenylboronic acid (S-PBA) was assembled onto the PAMAM-Au via the S-Au interaction, and then ARS was immobilized by S-PBA binding of cis-diol moieties, which was dropped on the surface of glassy carbon electrode as sensing platform to combine antibody. Meanwhile, amylase modified gold nanoparticles were employed as labels. Accompanying the sandwich immunoassay , the carried amylase could hydrolyze amylose into glucose, and the displacement-type format was triggered due to the stronger adhesion between glucose and PBA, which resulted in the change of electrochemical signals due to the decrease of ARS (as an electron mediator). Under optimal conditions, the SWV signals were related to the concentration of CEA, indicating a certain proportional relation in a range of 0.01~50 ng mL −1 with a detection limit (LOD) of 0.003 ng mL −1 . Intra- and inter-assay coefficients of variation were below 10%, respectively. In addition, the methodology showed good accordance with a commercialized enzyme-linked immunosorbent assay (ELISA) method.
研究领域:
生物化学
·
分析化学
·
癌症诊断
·
电化学传感
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产品关联
DOI
PubMed
高影响因子