ChemistrySelect
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2023
·Vol. 8
·期 2
·e202203646
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IF 2.1
Siying Ren,Wen-Chao Geng,Xuexian Cui,Bian Wu,Zhe Zheng
Graphical We present a robust supramolecular tandem assay to monitor L-DOPA decarboxylase activity and screen enzyme inhibitors using cucurbit[7]uril and acridine orange reporter pair. L–DOPA decarboxylase (DDC) deficiency causes serious progressive neurodegenerative disorders. Developing a sensitive enzyme activity monitoring and inhibitors or activators screening approach is highly on demand for DDC deficiency diagnosis. Here, we report a simple and sensitive fluorescence supramolecular tandem assay based on reporter pair of cucurbit[7]uril and acridine orange for DDC activity monitoring continuously. Furthermore, this strategy demonstrates the potential of STA to screen inhibitors of DDC.
研究领域:
生物化学
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医学诊断
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药物开发
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DOI
高影响因子
SENSORS AND ACTUATORS B-CHEMICAL
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2015
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IF 4.097
Weihua Zhu,Chenglei Xuan,Guoliang Liu,Zhuo Chen,Wei Wang
A simple fluorescent assay for sensing bovine serum albumin (BSA) and calf thymus DNA (ctDNA) was developed based on the gold nanorods-based probe. Gold nanorods coated with mesoporous silica coated (Au@SiO 2 ) which loading acridine orange (AO) was prepared by one-pot synthesis method. Interestingly, BSA is detected based on the quenching fluorescence signal while ctDNA is determined based on the enhanced fluorescence signal by the proposed method. Under the optimal conditions, the declined values of the fluorescent intensity of the biosensor are proportional to the BSA concentration in the range of 0.75–33.86 μmol/L. The limit of detection is 0.25 μmol/L. The enhanced values of the fluorescent intensity of the biosensor are linear with the ctDNA concentration in the range of 0.5–10 μg/mL, and the detection limit is 0.1667 μg/mL. The proposed method shows a good selectivity for BSA and ctDNA and can be applied to the determination of the analytes in real samples. The strategy of Au NRs@SiO 2 -AO complex as a novel fluorescent probe paves a new way to design fluorescent sensor.
研究领域:
分析化学
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生物传感
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纳米技术
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DOI
高影响因子
SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
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2023
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IF 4.4
Xinpeng Zhang,Xinyu Li,Danfeng Wang,Tianxin Weng,Lu Wang,Lixia Yuan,Qingpeng Wang,Jie Liu,Yushu Wu,Min Liu
Chemotherapy–phototherapy (CTPT) combination drugs co-loaded by targeted DNA nanostructures can achieve controlled drug delivery, reduce toxic side effects and overcome multidrug resistance. Herein, we constructed and characterized a DNA tetrahedral nanostructure (MUC1-TD) linked with the targeting aptamer MUC1. The interaction of daunorubicin (DAU)/acridine orange (AO) alone and in combination with MUC1-TD and the influence of the interaction on the cytotoxicity of the drugs were evaluated. Potassium ferrocyanide quenching analysis and DNA melting temperature assays were used to demonstrate the intercalative binding of DAU/AO to MUC1-TD. The interactions of DAU and/or AO with MUC1-TD were analyzed by fluorescence spectroscopy and differential scanning calorimetry. The number of binding sites, binding constant, entropy and enthalpy changes of the binding process were obtained. The binding strength and binding sites of DAU were higher than those of AO. The presence of AO in the ternary system weakened the binding of DAU to MUC1-TD. In vitro cytotoxicity studies demonstrated that the loading of MUC1-TD augmented the inhibitory effects of DAU and AO and the synergistic cytotoxic effects of DAU + AO on MCF-7 cells and MCF-7/ADR cells. Cell uptake studies showed that the loading of MUC1-TD was beneficial in promoting the apoptosis of MCF-7/ADR cells due to its enhanced targeting to the nucleus. This study has important guiding significance for the combined application of DAU and AO co-loaded by DNA nanostructures to overcome multidrug resistance.
研究领域:
纳米技术
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药学
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癌症研究
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分子生物学
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生物物理学
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DOI
PubMed
高影响因子
JOURNAL OF MOLECULAR LIQUIDS
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2022
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IF 6.633
Danfeng Wang,Min Liu,Yushu Wu,Tianxin Weng,Lu Wang,Yongfang Zhang,Yanna Zhao,Jun Han
The co-loading of chemotherapy-phototherapy (CTPT) combination drugs by aptamer-targeted DNA nanostructures has significant advantages in improving anticancer effects and overcoming the multidrug resistance of cancer cells. The different binding modes of drugs to DNA nanostructures may impact CTPT therapy. Here, the anti-drug resistance effects of idarubicin (IDA) or acridine orange (AO) as single drug, as well as IDA/mithramycin (MTR) dimers ((MTR) 2 Zn 2+ ) + AO combination drugs loaded by AS1411-tethered DNA nanotrains (AS1411NTrs), were studied. The intercalative binding mode between IDA/AO and AS1411NTrs was verified through measurements of viscosity, changes in melting temperature, and potassium iodide quenching. A series of thermodynamic parameters such as the binding constant and the number of binding sites were obtained through fluorescence spectroscopy, isothermal titration calorimetry, and differential scanning calorimetry. The high binding constants and the number of binding sites indicated that AS1411NTrs had a high loading capacity for IDA and AO. An in vitro release study showed that the release rate and release model of IDA/(MTR) 2 Zn 2+ /AO in the binary and ternary systems with or without deoxyribonuclease I were related to their binding mode and order of addition. An in vitro cytotoxicity study proved that the cytotoxicity and synergistic effects of the three drugs to human breast cancer MCF-7 cells and multidrug-resistant MCF-7/ADR cells were enhanced due to loading of AS1411NTrs. The IDA/(MTR) 2 Zn 2+ + AO combination drugs could more obviously enhance apoptosis of MCF-7/ADR cells as confirmed by cell apoptosis assays. The cell uptake study demonstrated that IDA/(MTR) 2 Zn 2+ /AO loaded by AS1411NTrs was mainly concentrated in the nucleus of MCF-7/ADR cells. This work will provide theoretical information for combination therapy of IDA/(MTR) 2 Zn 2+ and AO based on DNA nanostructures.
研究领域:
药学
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纳米技术
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癌症研究
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生物物理学
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分子生物学
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DOI
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
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2025
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IF 3.4
Ruijing Li,Weili Yang,Lijuan Zheng,Xingxue Yan,Cuihua Liu,Yaodong Zhang,Jitong Li
Prenatal alcohol exposure is a leading cause of developmental abnormalities and neurobehavioral deficits, collectively known as fetal alcohol spectrum disorder (FASD). The underlying molecular mechanisms, however, are not fully elucidated, hindering the development of effective therapeutic strategies. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a key pathological process in various diseases. Gastrodin (GAS), the primary bioactive component of Gastrodia elata , has demonstrated potent antioxidant and neuroprotective properties. This study aimed to investigate the protective effects of GAS against alcohol-induced developmental and neurotoxic damage and to elucidate the underlying molecular mechanisms. Using a zebrafish larval model, we found that exposure to 200 mM alcohol from 2 to 24 hours post-fertilization (hpf) induced significant developmental toxicity, including a decreased hatching rate, body length and eye diameter, and increased morphological malformations in larvae. Alcohol-exposed larvae also exhibited severe neurobehavioral deficits, characterized by a reduction in movement distance and average velocity in dark conditions. Mechanistically, alcohol exposure triggered ferroptosis, evidenced by an increase in intracellular Fe 2+ , malondialdehyde (MDA), and reactive oxygen species (ROS) levels, alongside a decrease in the levels of glutathione (GSH) and reduced glutathione peroxidase 4 (GPX4) and the nuclear factor erythroid 2-related factor 2 (Nrf2) activities. Co-treatment with GAS (200 mg/L) significantly ameliorated these alcohol-induced developmental and neurobehavioral defects. GAS administration effectively suppressed the hallmarks of ferroptosis by restoring the ROS level and altering the expression of genes related to oxidative stress. In addition, GAS suppressed alcohol-induced cell apoptosis, downregulated caspase3b , bax , caspase8 , and upregulated bcl2 in mRNA levels. Molecular analysis revealed that GAS exerts its anti-ferroptotic effect by activating Nrf2/GPX4 signaling pathway, which was suppressed by alcohol. Our findings indicate that ferroptosis plays a key role in alcohol-induced developmental neurotoxicity, and GAS provides protection by activating the Nrf2/GPX4 axis. This suggests that GAS could be a potential therapeutic option for reducing the negative effects of prenatal alcohol exposure.
研究领域:
神经毒理学
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发育生物学
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分子药理学
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氧化应激研究
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斑马鱼模型
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 6.8
Sheng-Ya Guo,Yong Zhang,Xing-Hui Chen,Yi-Wen Zhang,Bing-Bing Cao,Shi-Chang Zhu,Dao-Zong Xia
Ethnopharmacological relevance Smilax glabra Roxb. (taxonomically verified via http://www.theplantlist.org , accessed December 17, 2025), commonly known as “Tu fuling” in China, is a well-recognized traditional Chinese herb extensively used for detoxification, dampness relief, and diuresis. Our previous research has demonstrated that Smilax glabra flavonoids extract (SGF) alleviate lead (Pb)-induced renal damage. However, the protective effects of SGF against Pb-induced neurotoxicity and hematotoxicity remain largely uninvestigated, and the underlying molecular mechanisms have not been fully elucidated. Aim of the study To reveal the potential protective effects and underlying molecular mechanisms of SGF against Pb-induced neurotoxicity and hematotoxicity, a lead poisoned zebrafish model was utilized. Materials and methods Zebrafish were randomly divided into four groups: (a) control group (no treatment); (b) Pb group (exposed to 80 μM lead acetate); (c) positive control group (Pb + DMSA group: first exposed to 80 μM lead acetate, then separately exposed to 15.6 μg/mL DMSA); (d) Pb + SGF groups (first exposed to 80 μM lead acetate, then separately exposed to SGF at 31.2, 62.5, or 125 μg/mL). All zebrafish were subjected to the respective sequential treatments for 4 consecutive days. Results Our results showed that SGF significantly reduced Pb content in zebrafish. SGF treatment markedly alleviated a series of adverse effects induced by Pb exposure in zebrafish, including trunk curvature, shortened body length, peripheral motor neuron damage, myelin and axonal injury, neuronal apoptosis, neurobehavioral impairment, and anemia. Moreover, SGF treatment led to a significant decrease in ROS levels in Pb-exposed zebrafish. Mechanistic experiments demonstrated that SGF significantly upregulated the mRNA expression levels of nerve protection-related genes ( shha , gfap , mbp , and huc ), memory-related genes ( ache and gdnf ), and antioxidant-related genes ( nrf2 and cat ). Conversely, SGF predominantly downregulated the mRNA expression levels of inflammation-related genes ( il1β , il6 , and tnfα ) and apoptosis-related genes ( caspase 3 , bax , and p53 ). Meanwhile, SGF treatment significantly reduced the phospho-p65/p65 protein ratio. Conclusion These results suggest that SGF may mitigate acute Pb-induced neurotoxicity and hematotoxicity, and these protective effects are associated with enhanced Pb excretion and the inhibition of Pb-induced oxidative stress, inflammation, and apoptosis. Moreover, the neuroprotective and memory-improving effects of SGF were observed in conjunction with the regulation of neurotrophic factors. Our findings highlight the potential pharmacological value of SGF in counteracting lead poisoning. However, given that the acute high-dose model does not fully recapitulate chronic low-dose human exposure, further validation in chronic models is essential before translational conclusions can be drawn.
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PubMed
高影响因子
Science Advances
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2025
·Vol. 11
·期 17
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IF 12.5
Zhenggang Gong,Xianggang Weng,Deli Wu,Zhendong Lei,Guangxu Yang,Li Shuai
Increasing efforts have been devoted to developing biobased and biodegradable plastics and composites from lignocellulosic biomass. Current bioplastic production entails multiple challenging steps including monomer production from biomass as well as polymer synthesis and modification. Here, we report a practical recombination strategy to transform agricultural residues into moldable cellulose-reinforced lignin (CRL) composites. The strategy involves deconstruction of biomass particles followed by thermo-compression molding of cellulose fibers and lignin mixtures. The resulting CRL composites demonstrated excellent mechanical and thermal properties as well as water, abrasive, and flame resistance. Mechanistic studies reveal that small particle size, removal of water-soluble fractions, as well as reservation of lignin and its cross-linking reactivity have considerably positive effects on preparation of high-quality composite items. These insights offer a versatile strategy for transforming various types of low-grade biomass, such as corn stover, into eco-friendly and potentially biodegradable or compostable composites that can serve as sustainable alternatives to traditional duroplast materials.
研究领域:
材料科学
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生物工程
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DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
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2025
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IF 7.3
Yiyun Liu,Qi-Ping Tang,Si-Jia Zuo,Yuan Ding,Feng-Yi Guo,Bao-Fu Zhang,Qin-Hong Zhou,Dongmei Xie,De-Sheng Pei
The surge in global plastic usage has exacerbated the pollution of nanoplastics and plasticizers in aquatic ecosystems, causing widespread concern about population health issues. We used a zebrafish model to investigate the combined toxicity of polystyrene nanoparticles (PS-NPs) and plasticizer metabolite mono-(2-ethylhexyl) phthalate (MEHP), revealing the synergistic neurotoxic effects and potential mechanisms of compound exposure. Co-exposure amplifies the bioaccumulation of PS-NPs ( p < 0.05), causing innate immune damage ( p < 0.0001), severe oxidative stress ( p < 0.0001), and embryonic apoptosis ( p < 0.05), while inducing larval neuromotor dysfunction and changes in neural markers. Further exploration revealed that oxidative stress-induced lipid peroxidation disrupts glycerophospholipid metabolism and cholinergic synthesis, which can be an important mechanism for neurotoxicity caused by the co-exposure of PS-NPs and MEHP. This hypothesis is supported by dysregulation of acetylcholinesterase ( ache ), docking protein 7 ( dok7 ), and heparan sulfate proteoglycan 2 ( hspg2 ) genes linked to neurotransmission. In summary, this study reveals new synergistic toxicity mechanisms between nanoplastics and plasticizers, advancing the risk assessment framework for complex environmental pollutant interactions.
研究领域:
生态毒理学
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环境科学
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神经生物学
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DOI
PubMed
高影响因子
JOURNAL OF MATERIALS SCIENCE
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2025
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IF 3.9
Wang Xi,Wu Juan,Sun Haibin,Lu Bingyan,Huang Jingjing,Liu Qiaoling,Li Tingting
Biofilms pose a significant challenge to public health, fostering persistent infections that are notoriously difficult to eradicate. Their resilience stems partly from the inadequate penetration of conventional antibacterial agents into these structured microbial communities. To address this issue, we have developed a novel magnetite iron oxide Janus nanoparticles (JNPs), harnessing the magnetic field assistance for targeted biofilm elimination. In which, natural tannic acid (TA) and chitosan (CS) were coated on IONPs for improved antibacterial property and biocompatibility. Subsequently, the surfaces were functionalized with epoxy chloropropane and butanediamine, creating anchor points for the deposition of silver nanoparticles (AgNPs). Subsequently, AgNPs were embedded via an in situ reduction process, utilizing polyvinyl pyrrolidone (PVP) to precisely control the morphology of the Ag-armed magnetite JNPs. Remarkably, IONPs@BCS/Ag exhibited dual-responsive release characteristics, sensitively adjusting their Ag + release in response to both oxygen levels and pH variations within the biofilms microenvironment. This system leveraged both stimulus-responsiveness and magnetic guidance to deliver exceptional antimicrobial performance against both planktonic bacteria and established biofilms. Critically, the superparamagnetic nature of IONPs@BCS/Ag enabled enhanced penetration into biofilms under an external magnetic field, facilitating the efficient delivery of AgNPs. Furthermore, the sustained release of Ag + triggered by low pH and oxygen levels within the biofilm triggered the generation of reactive oxygen species (ROS), which not only accelerated the decomposition of the biofilm matrix but also disrupted the integrity of microbial communities. In summary, the IONPs@BCS/Ag magnetite JNPs, augmented by an external magnetic field, demonstrated enhanced anti-biofilm capabilities, offering immense potential as a potent weapon against biofilm-associated infections. Graphical abstract
研究领域:
材料科学
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微生物学
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医学工程
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DOI
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2024
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IF 6.2
Ruijing Li,Weili Yang,Xingxue Yan,Xinkui Zhou,Xiaorui Song,Cuihua Liu,Yaodong Zhang,Jitong Li
Bisphenol A (BPA) is a widespread environmental endocrine disruptor (EED) that can cause various environmental and health issues by inducing oxidative stress. The c-Jun N-terminal kinase (JNK) signaling pathway plays a crucial role in oxidative stress-mediated cellular damage. Although folic acid (FA) has demonstrated antioxidant properties, its potential protective effects against BPA-induced developmental and neurotoxicity, as well as the mechanisms involved in the JNK signaling pathway, are still not completely understood. Zebrafish embryos were exposed to different concentrations of BPA ranging from 20 to 40 µM, with or without treatment of 50 µM FA, starting at 6 hours post-fertilization (hpf). Various parameters such as hatchability, survival rate, body length, and heart rate were measured and analyzed. Transcriptome sequencing was conducted to study the changes in gene expression. Oxidative stress markers, including reactive oxygen species (ROS), lipid peroxidation (LPO), hydrogen peroxide (H 2 O 2 ), and catalase (CAT) activity, were assessed. The expression of proteins related to the mitogen-activated protein kinase (MAPK)/JNK pathway was analyzed using western blot. Neurodevelopmental and apoptotic outcomes were evaluated through behavioral tests, immunofluorescence and RT-qPCR examinations. The study found that exposure to BPA led to a decrease in hatchability, survival, body length, heart rate, total antioxidant capacity and promoted apoptosis in zebrafish larvae. However, supplementation with FA was able to alleviate these negative effects. BPA exposure increased levels of ROS, LPO, and H 2 O 2 , while decreasing CAT activity in zebrafish larvae. Treatment with FA effectively reduced BPA-induced oxidative stress and restored antioxidant defense systems. Moreover, KEGG pathway enrichment analysis revealed that the MAPK signaling pathway was the most enriched signaling pathway. Further studies revealed that BPA activated the JNK signaling pathway, while FA suppressed this activation. Additionally, FA significantly improved BPA-induced neurobehavioral deficits and protected against neurocytological alterations. Our findings demonstrate that FA effectively protects against BPA-induced developmental and neurotoxic effects in zebrafish by suppressing oxidative stress and inhibiting the JNK signaling pathway. This study provides new strategies and insights for preventing BPA-induced developmental and neurotoxicity in aquatic organisms.
研究领域:
环境科学
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毒理学
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发育生物学
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神经科学
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DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2024
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IF 3.9
Yue Tao,Xiaodong Yi,Yanyan Gu,Rongyi Yang,Zixu Li,Xiangyong Guo,Donglin Zhao,Ying Zhang
This work was designed to investigate the neurotoxic effects of the typical plasticizer dibutyl phthalate (DBP) using zebrafish larvae as a model. The results of exhibited that zebrafish larvae exposed to DBP at concentrations of 5 μg/L and 10 μg/L exhibited brain malformations (24 h) and behavioral abnormalities (72 h). After 72 h of exposure to DBP, microglia in the brain were over-activated, reactive oxygen species (ROS) formation was increased, and apoptosis was observed. Meanwhile, it was found that neurons exhibited impaired mitochondrial structure, absent mitochondrial membrane potential and up-regulated autophagy. Further comprehensive biochemical analyses and RNA-Seq, validated by RT-qPCR, glutamate metabolism and PPAR signaling pathway were significantly enriched in the DBP stress group, this may be the main reason for the disruption of glycolysis/gluconeogenesis processes and the reduction of energy substrates for the astrocyte-neuron lactate shuttle (ANLS). In addition, the DBP-exposed group showed aberrant activation of endoplasmic reticulum (ER) stress signaling pathway, which may be related to ROS as well as neuronal apoptosis and autophagy. In conclusion, DBP-induced neurotoxicity may be the combined result of insufficient neuronal energy acquisition, damage to mitochondrial structure, apoptosis and autophagy. These results provide a theoretical basis for understanding the neurotoxic effects of DBP.
研究领域:
毒理学
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神经科学
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环境科学
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分子生物学
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DOI
PubMed
高影响因子
Materials Science & Engineering C-Materials for Biological Applications
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2016
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IF 3.42
Juan Wu,Wei Jiang,Yewen Shen,Wei Jiang,Renbing Tian
Multifunctional nanocarriers based on the Fe 3 O 4 nanoparticles core and mesoporous silica shell (mSiO 2 ) were synthesized for controlled drug release through magnetic targeting and pH-sensitive performances. The developed Fe 3 O 4 @mSiO 2 nanocarriers exhibited a suitable size (63 nm) and good magnetic responsibility, doxorubicin (DOX) could be successfully loaded into the mesoporous of Fe 3 O 4 @mSiO 2 via electrostatic interaction, and the drug loading content and loading efficiency are 29.3% and 93.6%, respectively. The chitosan (CS) was employed to wrap the Fe 3 O 4 @mSiO 2 -DOX as the blocking agent to inhibit premature drug release, and the final CS/Fe 3 O 4 @mSiO 2 -DOX exhibited excellent pH-sensitivity, 86.1% DOX was released within 48 h at pH 4.0. Furthermore, all the release behaviors fit the Higuchi model very well and a purely diffusion-controlled process played a major role on DOX release from CS/Fe 3 O 4 @mSiO 2 -DOX. In addition, MTT assays in human liver hepatocellular carcinoma cells (HepG2) demonstrated that the CS/Fe 3 O 4 @mSiO 2 -DOX had high anti-tumor activity, while the Fe 3 O 4 @mSiO 2 nanocarriers were practically non-toxic. Thus, our results revealed that the CS/Fe 3 O 4 @mSiO 2 -DOX could play an important role in the development of intracellular delivery nanodevices for cancer therapy.
研究领域:
材料科学
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药物递送
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肿瘤学
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DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）