Materials Today Bio
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2025
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IF 10.2
Fugen Wu,Xing Xia,Yuqi Han,Zihao Huang,Yitianhe Xu,Zihao Tao,Yunzhi Wang,Dingchao Shen,Shengnan Song,Wanling Zhu,Ruijie Chen,Xianbao Shi,Xinyu Jiang,Longfa Kou
Psoriasis is a chronic skin disorder characterized by dysregulation of immune and epithelial cells, resulting in persistent symptoms such as erythema, scaling, and induration. The abnormal metabolism and increased oxidative stress in psoriasis lesions have been identified as key drivers in the pathogenesis of psoriasis, forming a positive feedback loop within psoriatic skin. Therefore, targeting this feedback loop through modulation of local metabolism and alleviation of oxidative stress could be a rational and promising therapeutic strategy for addressing psoriasis. Herein, we designed a carrier-free nanomedicine (BTN) incorporating bilirubin (BR) and triptolide (TPL) to specifically target two key pathological features of psoriasis: inflammation induced by enhanced reactive oxygen species (ROS) and aberrant proliferation/immune activation driven by heightened nutrient metabolism. In vitro studies demonstrated that BTN effectively improved the water solubility of BR and TPL while facilitating efficient drug delivery to inflammatory keratinocytes. Mechanistically, BTN was found to alleviate the inflammatory cascade caused by oxidative stress and inhibit the IL-23/IL-17 axis. Importantly, downregulation of HIF-1α in keratinocytes resulted in blocking glucose transportation via GLUT-1 as well as amino acid transportation via LAT1, ultimately impeding excessive proliferation by disrupting nutritional requirements. In an imiquimod-induced psoriasis model, BTN effectively permeated inflamed skin epithelium with long-term retention effect. As a multifunctional nanomedicine combining ROS scavenging properties with regulation of nutrition metabolism, BTN shows great promise for reducing inflammatory cell infiltration and suppressing keratinocyte proliferation. Our findings demonstrated the great potential of BTN in ameliorating psoriasis symptoms by restoring the metabolic imbalance and mitigating oxidative stress between the epithelial and immune compartments.
研究领域:
皮肤病学
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药理学
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免疫学
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产品关联
DOI
PubMed
高影响因子
Micromachines
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2022
·Vol. 13
·期 1
·83
·
IF 3.523
Kai Guo,Zirui Song,Gaoxing Wang,Chengchun Tang
Microbial activity has gained attention because of its impact on the environment and the quality of people’s lives. Most of today’s methods, which include genome sequencing and electrochemistry, are costly and difficult to manage. Our group proposed a method using the redox potential change to detect microbial activity, which is rooted in the concept that metabolic activity can change the redox potential of a microbial community. The redox potential change was captured by a biosensor consisting of porous boron nitride, ATP-DNA aptamer, and methylene blue as the fluorophore. This assembly can switch on or off when there is a redox potential change, and this change leads to a fluorescence change that can be examined using a multipurpose microplate reader. The results show that this biosensor can detect microbial community changes when its composition is changed or toxic metals are ingested.Keywords:redox potential;aptamer;dysbiosis;boron nitride;fluorescence
研究领域:
环境科学
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生物技术
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微生物学
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电化学
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产品关联
DOI
PubMed
高影响因子
Advanced Science
·
2025
·
IF 14.1
Yong Zhu,Ziqu Fang,Jie Bai,Longhui Wang,Jiaqing Chen,Zehua Zhang,Qiang Wang,Weiwei Sheng,Xueyin Pan,Zhenyuan Gao,Dengqiu Xu,Pengkai Wu,Beicheng Sun
Maintaining microbiota balance and enhancing the antioxidant performance of nanozyme-based probiotic systems are crucial for effective inflammatory bowel disease (IBD) therapy. Despite significant advancements, developing a green and safe coating technology that functionalizes probiotics with nanozymes while preserving the activity of both components remains a challenge. To address this, chitosan-modified epigallocatechin gallate (EGCG-CS, EC)is synthesized, leveraging the intrinsic adhesive and coordination properties of polyphenols to capture gold nanozymes (AuNPs), forming ECA complexes that enhance nanozyme activity. When coated onto Escherichia coli Nissle 1917 (EcN), the resulting ECA@EcN system effectively scavenged reactive oxygen species (ROS), improving probiotic viability and promoting colon accumulation. Mechanistically, ECA protected EcN by suppressing the activation of the Flagellar Assembly and Branched-Chain Amino Acid Synthesis pathways, ultimately alleviating inflammation and modulating intestinal microbial communities to relieve IBD symptoms. Given the biocompatibility of its components and the environmentally friendly assembly approach, this polyphenol-nanozyme-armored probiotic system represents a promising platform for IBD treatment.
研究领域:
生物医学工程
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消化病学
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纳米医学
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DOI
PubMed
高影响因子
iScience
·
2021
·
IF 5.458
Yanhong Hao,Zheng Zhang,Guifang Feng,Moran Chen,Qiongqiong Wan,Jie Lin,Liang Wu,Wenjing Nie,Suming Chen
Summary Asymptomatic infection is a big challenge in curbing the spread of COVID-19. However, its identification and pathogenesis elucidation remain issues. Here, by performing comprehensive lipidomic characterization of serum samples from 89 asymptomatic COVID-19 patients and 178 healthy controls, we screened out a panel of 15 key lipids that could accurately identify asymptomatic patients using a new ensemble learning model based on stacking strategy with a voting algorithm. This strategy provided a high accuracy of 96.0% with only 3.6% false positive rate and 4.8% false negative rate. More importantly, the unique lipid metabolic dysregulation was revealed, especially the enhanced synthesis of membrane phospholipids, altered sphingolipids homeostasis, and differential fatty acids metabolic pattern, implicating the specific host immune, inflammatory, and antiviral responses in asymptomatic COVID-19. This study provides a potential prediagnostic method for asymptomatic COVID-19 and molecular clues for the pathogenesis and therapy of this disease.
研究领域:
医学
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生物信息学
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免疫学
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DOI
高影响因子
CHEMOSPHERE
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2023
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IF 8.8
Zelong Zhao,Xuda Wang,Jingwei Jiang,Ying Dong,Yongjia Pan,Xiaoyan Guan,Bai Wang,Shan Gao,Zhong Chen,Zunchun Zhou
The mariculture environment is a sink of microplastics (MPs) due to its enclosed nature and mass use of plastics. Nanoplastics (NPs) are MPs with a diameter <1 μm that have a more toxic effect on aquatic organisms than other MPs. However, little is known about the underlying mechanisms of NP toxicity on mariculture species. Here, we performed a multi-omics investigation to explore gut microbiota dysbiosis and associated health problems induced by NPs in juvenile sea cucumber Apostichopus japonicus , a commercially and ecologically important marine invertebrate. We observed significant differences in gut microbiota composition after 21 days of NP exposure. Ingestion of NPs significantly increased core gut microbes, especially Rhodobacteraceae and Flavobacteriaceae families. Additionally, gut gene expression profiles were altered by NPs, especially those related to neurological diseases and movement disorders. Correlation and network analyses indicated close relationships between transcriptome changes and gut microbiota variation. Furthermore, NPs induced oxidative stress in sea cucumber intestines, which may be associated with intraspecies variation in Rhodobacteraceae in the gut microbiota. The results suggested that NPs were harmful to the health of sea cucumbers, and they highlighted the importance of the gut microbiota in the responses to NP toxicity in marine invertebrates.
研究领域:
环境科学
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海洋生物学
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微生物学
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DOI
PubMed
高影响因子
Environmental Chemistry and Ecotoxicology
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2025
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IF 8.2
Bin Liu,Cun-Long Wang,Teng-Zhou Li,Jian-Xue Feng,Yu-Qing Ma,Ling Liu,Ping Li,Zhi-Hua Li
Tralopyril has emerged as a promising alternative to the banned tributyltin in marine antifouling applications. However, its ecological risks remain underestimated. Through an integrated approach combining behavioral phenotyping, transcriptomics, and whole-genome bisulfite sequencing (WGBS), we demonstrate that tralopyril (0, 1, 10 μg/L) disrupts marine medaka ( Oryzias melastigma) development via two interrelated mechanisms: (1) Epigenetic dysregulation: Aberrant CG methylation in key regulatory genes ( casr , cacna2d2 , dnai1 , alox15b , etc.) was associated with developmental toxicity, altering gene expression profiles critical for normal growth. (2) Ferroptosis activation: Tralopyril exposure triggered iron overload and fth1 dysregulation, while mitochondrial uncoupling ( ucp2 ) exacerbated oxidative stress, contributing to cellular damage. Notably, epigenetic alterations, such as methylation changes in alox15b , can influence the ferroptosis pathway by regulating genes involved in iron metabolism and oxidative stress. This, in turn, amplified toxic effects and contributed to multiorgan damage. These alterations led to defects such as cardiac remodeling, skeletal malformations, and neuromuscular dysfunction, ultimately resulting in locomotor decline. Inhibitor rescue experiments identified critical molecular targets of tralopyril's toxic effects and demonstrated cross-regulation between ucp2 expression and the ferroptosis pathway. These findings elucidate the key molecular mechanisms underlying tralopyril-induced developmental abnormalities and behavioral impairments, emphasizing the synergistic effects of mitochondrial dysfunction and ferroptosis. Overall, this study expands the understanding of mitochondrial function and ferroptosis in environmental toxicology and provides a scientific basis for ecological risk assessment and mitigation strategies for environmental pollutants.
研究领域:
环境毒理学
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分子生物学
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生态学
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产品关联
DOI
高影响因子
mSystems
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2024
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IF 5
Jiaming Zhang,Xiaoxia Yu,Weidong Li,Yunjing Jiang,Liangran Zhang,Shunxin Wang
A good quality egg is essential for a successful pregnancy and early embryo development. Oocyte development is vulnerable to environmental exposures. Bisphenol S (BPS) is widely used as a replacement for its analog bisphenol A, but the reproductive toxicity of BPS has been of great concern. In this study, we showed that BPS exposure induces dysbiosis of the gut microbiota, which further leads to intestinal permeability and inflammation, and ultimately impairs oocyte quality. More importantly, we found that alginate oligosaccharide reshapes the gut microbiota to improve gut homeostasis, thereby preventing the deleterious effects of BPS on the gut and oocytes. Overall, this study not only demonstrates that BPS exposure impairs the intestine and oocytes by inducing dysbiosis of the gut microbiota but also develops a preventive strategy.
研究领域:
生殖生物学
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环境毒理学
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微生物学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL SCIENCE & TECHNOLOGY
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2025
·
IF 11.3
Huaying Liu,Qisong Xing,Chenyu Zhu,Qineng Wang,Keding Lu,Song Guo,Zhijun Wu,Min Hu,Shao-Meng Li,Maosheng Yao
Endotoxin (lipopolysaccharide, LPS), widely distributed in the atmospheric environment with strong immunogenicity, is an important biological component of ambient particulate matter. However, whether LPS participates in atmospheric chemistry and how its biological health impacts change with the relevant processes are poorly understood. In this study, we employed the rat model to investigate the impact of ozone oxidation on the biological toxicity of LPS and used Fourier transform infrared spectroscopy and high-resolution electrospray mass spectrometry to study the underlying reaction mechanisms. The results show that the LPS can be oxidized by ozone and the resulting reactant greatly enhanced inflammatory anemia with a 177% capacity increase despite a minor influence on its immunogenicity. In contrast to the control, rats exposed to oxidized LPS were observed to release characteristic exhaled biomarkers, indicating that the formed reactant indeed altered the biological effects of LPS. Mechanistic investigation reveals that ozone oxidation of the hydroxyl group in the key toxic part of LPS, kdo2-lipid A, can cause dysregulation of iron homeostasis in rats, which is the mechanism of oxidized LPS-enhanced anemia. Unfortunately, these chemical structure changes and the resulting health impacts cannot be detected by the conventional LPS analysis method. This study highlights the changes in the toxicity of LPS and its health impacts when oxidized by ozone and the need to broadly consider the involvement of bioaerosol in atmospheric chemistry.
研究领域:
环境生物学
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毒理学
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医学
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产品关联
DOI
PubMed
高影响因子
SCIENCE OF THE TOTAL ENVIRONMENT
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2022
·
IF 10.753
Yang Wang,Jie Song,Xuedong Wang,Qiuhui Qian,Huili Wang
Triclosan (TCS), as a broad-spectrum bactericide, is extensively used in the fine chemical and textile industries. It is recognized as a new type of environmental endocrine disruptor with frequent detection and environmental pollution. However, the toxicity mechanism regarding neurodevelopment and neurobehavior remains unclear. This study is intended to explore the underlying toxic mechanism of TCS based on gut-brain axis. TCS-chronic exposure affected the development of zebrafish, induced feminization, obesity physical signs and abnormal organ index and caused neurobehavioral abnormalities by inhibiting both neurotransmitter acetylcholinesterase and dopamine activity, promoting brain neuron apoptosis and accelerating diencephalic lesions. Meanwhile, TCS-chronic exposure led to gut microbiota dysbiosis and decreased diversity, such as increased pathogenic bacteria and decreased probiotics in adult zebrafish gut, which caused many pathological damages, including partial shedding and ablation of intestinal villi, inflammatory infiltration, thinning of intestinal wall, and increased goblet cell in villus. Based on the communication between intestinal peripheral nerves and CNS, the above histopathological injuries and disorders were well underpinned and illustrated by the changes of biomarkers and the expression of related marker genes in the gut-brain axis. Additionally, short-chain fatty acids (SCFA), as the regulators of intestinal sympathetic nerve activation, are also secreting products of intestinal microflora and play a crucial role in regulating the balance of intestinal flora and protecting intestinal homeostasis. SCFA in low doses can effectively alleviate and rescue the toxic effects under TCS exposure, which evidenced that TCS exerted systemic toxic effects on the gut-brain axis by influencing the composition and diversity of gut flora in zebrafish, and fully demonstrated the interaction effect between intestine and brain. Hence, these findings contribute to the understanding, prevention, and diagnosis of endocrine disrupting diseases caused by environmental pollutants from the perspective of the gut-brain axis, and strengthening the early warning, management and control of TCS pollution.
研究领域:
环境科学
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毒理学
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神经生物学
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DOI
PubMed
高影响因子
Microorganisms
·
2021
·Vol. 9
·期 8
·1742
·
IF 4.128
Zihan Zhang,Chao Xue,Mengyao Ju,Jiawei Guo,Minghui Wang,Sijie Yi,Xianfeng Yi
Increasing application of antibiotics changes the gut microbiota composition, leading to dysbiosis of the gut microbiota. Although growing evidence suggests the potential role of gut dysbiosis as the cause of neurodevelopmental disorders and behavioral defects, a broad gap of knowledge remains to be narrowed to better understand the exact mechanisms by which maternal gut dysbiosis alters microbiota development and social interactions of offspring. Here, we showed that maternal gut dysbiosis during gestation is a critical determinant of gut microbiota and social interactions off mouse offspring. Gut microbiota of 2-week-old offspring showed significant changes in response to maternal antibiotic treatment. We even detected distinct effects of maternal oral antibiotics on gut microbiota of 14-week-old offspring. Compared to controls, offspring born to antibiotics-treated mothers displayed reduction in sociability and preference for social novelty, suggesting that the altered offspring social behavior was closely linked to dysbiosis of maternal gut microbiota. Our study opens the possibility to better understand the mechanism of how maternal gut microbiota vertically impairs social interactions of offspring in animal models, providing support to the maternal gut microbiota as a potential mediator between offspring microbiota and behaviors.Keywords:maternal gut dysbiosis;antibiotics;offspring;gut microbiota;metabolome;social behavior
研究领域:
微生物学
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神经科学
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发育生物学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Microbiology
·
2023
·
IF 5.2
Haisu Liu,Hang Zhang,Qianxun Yu,Sanshan Zhang,Xiao Tu,Fenghong Zhuang,Shengli Fu
Lead (Pb) is a hazardous pollutant in water environments that can cause significant damage to aquatic animals and humans. In this study, crucian carp ( Carassius auratus ) were exposed to waterborne Pb for 96 h; then, histopathological analysis, quantitative qPCR analysis, and 16S high-throughput sequencing were performed to explore the effects of Pb on intestinal bioaccumulation, structural damage, oxidative stress, immune response, and microbiota imbalance of C. auratus . After Pb exposure, the intestinal morphology was obviously damaged, including significantly increasing the thickness of the intestinal wall and the number of goblet cells and reducing the depth of intestinal crypts. Pb exposure reduced the mRNA expressions of Claudin-7 and villin-1 while significantly elevated the level of GST, GSH, CAT, IL-8, IL-10, IL-1 , and TNF- α. Furthermore, 16S rRNA analysis showed that the Shannon and Simpson indices decreased at 48 h after Pb exposure, and the abundance of pathogenic bacteria (Erysipelotrichaceae, Weeksellaceae, and Vibrionaceae) increased after Pb exposure. In addition, the correlation network analysis found that Proteobacteria were negatively correlated with Firmicutes and positively correlated with Bacteroidetes . Functional prediction analysis of bacteria speculated that the change in intestinal microbiota led to the PPAR signaling pathway and peroxisome function of the intestine of crucian carp was increased, while the immune system and membrane transport function were decreased. Finally, canonical correlation analysis (CCA) found that there were correlations between the intestinal microbiota, morphology, antioxidant factors, and immune factors of crucian carp after Pb exposure. Taken together, our results demonstrated that intestinal flora dysbiosis, morphological disruption, oxidative stress, and immune injury are involved in the toxic damage of Pb exposure to the intestinal structure and function of crucian carp. Meanwhile, Pb exposure rapidly increased the abundance of pathogenic bacteria, leading to intestinal disorders, further aggravating the damage of Pb to intestinal structure and function. These findings provide us a basis for the link between gut microbiome changes and heavy metal toxicity, and gut microbiota can be used as biomarkers for the evaluation of heavy metal pollution in future.
研究领域:
环境科学
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水产养殖学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2025
·
IF 5.6
Shanhui Zhang,Fuhui Zhao,Changluan Pan,Yajing Wang,Zhangxiang Yang,Jing Yang,Yunniao Meng,Shaofang Lv,Jiayu Huang,Li Dong,Lei Li,Yongxi Dong
Type 2 diabetes (T2DM), which is characterized by insulin resistance and diminished sensitivity, accounts for more than 90 % of the incidence rate of diabetes. At present, the drugs used to treat T2DM in clinic are restricted due to their poor compliance or serious adverse reactions. The abnormally elevated activity of GSK-3β plays an important regulatory role in the occurrence and development of T2DM. Herein, we report the therapeutic effect of a GSK-3β covalent inhibitor N -(3-(4-benzyl-3,5-dioxo-1,2,4-thiadiazol-2-yl) phenyl) acrylamide ( GL10a ), which was discovered by our group with excellent inhibitory activity and homologous kinase selectivity. Further research had confirmed that GL10a could inhibit the activity of GSK-3β, thereby increasing the hepatic glycogen synthesis, restoring glucose homeostasis, regulating insulin signaling pathways, and improving pancreatic β-cell function with consequent increase in insulin secretion. Additionally, our findings revealed that GL10a exerted beneficial effects on gut microbiota dysbiosis in T2DM, which may contribute to its therapeutic efficacy and facilitate disease recovery. These comprehensive pharmacological properties positioned GL10a as a promising candidate, potentially offering novel therapeutic strategies and clinical options for T2DM management.
研究领域:
药理学
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代谢疾病
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分子生物学
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药物开发
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转化医学
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）