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Controlling heavy metal pollution in agricultural soil has been a significant challenge. These heavy metals seriously threaten the surrounding ecological environment and human health. The effective assessment and remediation of heavy metals in agricultural soils are crucial. These two aspects support each other, forming a close and complete decision-making chain. Therefore, this review systematically summarizes the distribution characteristics of soil heavy metal pollution, the correlation between soil and crop heavy metal contents, the presence pattern and migration and transformation mode of heavy metals in the soil-crop system. The advantages and disadvantages of the risk evaluation tools and models of heavy metal pollution in farmland are further outlined, which provides important guidance for an in-depth understanding of the characteristics of heavy metal pollution in farmland soils and the assessment of the environmental risk. Soil remediation strategies involve multiple physical, chemical, biological and even combined technologies, and this paper compares the potential and effect of the above current remediation technologies in heavy metal polluted farmland soils. Finally, the main problems and possible research directions of future heavy metal risk assessment and remediation technologies in agricultural soils are prospected. This review provides new ideas for effective assessment and selection of remediation technologies based on the characterization of soil heavy metals.
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Agricultura , Monitoreo del Ambiente , Restauración y Remediación Ambiental , Metales Pesados , Contaminantes del Suelo , Suelo , Metales Pesados/análisis , Contaminantes del Suelo/análisis , Restauración y Remediación Ambiental/métodos , Agricultura/métodos , Medición de Riesgo , Suelo/química , Contaminación AmbientalRESUMEN
Developing surfaces that effectively repel low-surface-tension liquids with tunable adhesive properties remains a pivotal challenge. Micronano hierarchical re-entrant structures emerge as a promising solution, offering a robust structural defense against liquid penetration, minimizing area fraction, and creating narrow gaps that generate substantial upward Laplace pressure. However, the absence of an efficient, scalable, and tunable construction method has impeded their widespread applications. Here, drawing inspiration from springtail epidermal structures, octopus suckers, and rose petals, we present a scalable manufacturing strategy for artificial micronano hierarchical T-shaped structures. This strategy employs double-transfer UV-curing nanoimprint lithography to form nanostructures on microstructured surfaces, offering high structural tunability. This approach enables precise control over topography, feature size, and arrangement of nano- and microscale sections, resulting in superamphiphobic surfaces that exhibit high contact angles (>150°) and tunable adhesive forces for low-surface-energy liquids. These surfaces can be applied to droplet-based microreactors, programmable droplet-transfer systems, and self-cleaning surfaces suitable for various liquids, particularly those with low surface tension. Remarkably, we have also succeeded in fabricating the hierarchical structures on flexible and transparent substrates. We demonstrate the advantages of this strategy in the fabrication of hierarchical micronanostructures, opening up a wide range of potential applications.
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Ferroptosis, an emerging type of programmed cell death, is initiated by iron-dependent and excessive ROS-mediated lipid peroxidation, which eventually leads to plasma membrane rupture and cell death. Many canonical signalling pathways and biological processes are involved in ferroptosis. Furthermore, cancer cells are more susceptible to ferroptosis due to the high load of ROS and unique metabolic characteristics, including iron requirements. Recent investigations have revealed that ferroptosis plays a crucial role in the progression of tumours, especially HCC. Specifically, the induction of ferroptosis can not only inhibit the growth of hepatoma cells, thereby reversing tumorigenesis, but also improves the efficacy of immunotherapy and enhances the antitumour immune response. Therefore, triggering ferroptosis has become a new therapeutic strategy for cancer therapy. In this review, we summarize the characteristics of ferroptosis based on its underlying mechanism and role in HCC and provide possible therapeutic applications.
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Carcinoma Hepatocelular , Ferroptosis , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patología , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patología , Especies Reactivas de Oxígeno/metabolismo , Animales , Peroxidación de Lípido , Transducción de Señal , Hierro/metabolismoRESUMEN
Posttraumatic stress disorder (PTSD) is a complex mental disorder notable for traumatic experience memory. Although current first-line treatments are linked with clinically important symptom reduction, a large proportion of patients retained to experience considerable residual symptoms, indicating pathogenic mechanism should be illustrated further. Recent studies reported that newly formed myelin could shape neural circuit function and be implicated in fear memory preservation. However, its role in PTSD remains to be elucidated. In this study, we adopted a restraint stress-induced PTSD mouse model and found that PTSD-related neuropsychiatric symptoms were accompanied by increased myelination in the posterior parietal cortex and hippocampus. Fluoxetine, but not risperidone or sertraline, has a more profound rescue effect on neuropsychological behaviors and myelin abnormalities. Further mechanistic experiments revealed that fluoxetine could directly interfere with oligodendroglial differentiation by upregulating Wnt signaling. Our data demonstrated the correlation between PTSD and abnormal myelination, suggesting that the oligodendroglial lineage could be a target for PTSD treatment.
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Modelos Animales de Enfermedad , Fluoxetina , Ratones Endogámicos C57BL , Vaina de Mielina , Trastornos por Estrés Postraumático , Animales , Trastornos por Estrés Postraumático/tratamiento farmacológico , Fluoxetina/farmacología , Fluoxetina/uso terapéutico , Vaina de Mielina/efectos de los fármacos , Vaina de Mielina/patología , Vaina de Mielina/metabolismo , Masculino , Ratones , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Oligodendroglía/efectos de los fármacos , Oligodendroglía/metabolismo , Lóbulo Parietal/efectos de los fármacos , Vía de Señalización Wnt/efectos de los fármacos , Inhibidores Selectivos de la Recaptación de Serotonina/farmacologíaRESUMEN
METTL3-mediated N6-methyladenosine (m6A) modification is critical for gametogenesis and early embryonic development. However, the function of METTL3-mediated m6A modification in the early development of somatic nuclear transfer embryos (SCNT) remains unclear. Here, we found that METTL3 mRNA and protein levels exhibit dynamic changes during the early development of porcine SCNT embryos. The levels of METTL3 mRNA and protein in SCNT embryos at specific developmental stages differ from those in parthenogenetic activation (PA) counterparts. SiRNA injection effectively reduced the levels of METTL3 mRNA and protein in 4-cell embryos and blastocysts. METTL3 knockdown significantly reduced the cleavage and blastocyst rates of SCNT embryos. METTL3 knockdown significantly reduced the number of total cells and trophectoderm (TE) cells in the resulting blastocysts and perturbed cell lineage allocation. In addition, METTL3 knockdown reduced the levels of m6A modification in 4-cell embryos and blastocysts. Importantly, METTL3 knockdown decreased the expression levels of CDX2, GATA3, NANOG and YAP, and increased the expression levels of SOX2 and OCT4. Taken together, these results demonstrate that METTL3-mediated m6A modification regulates early development and lineage differentiation of porcine SCNT embryos.
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Clonación de Organismos , Desarrollo Embrionario , Regulación del Desarrollo de la Expresión Génica , Metiltransferasas , Animales , Porcinos/embriología , Porcinos/genética , Metiltransferasas/genética , Metiltransferasas/metabolismo , Clonación de Organismos/veterinaria , Clonación de Organismos/métodos , Técnicas de Transferencia Nuclear/veterinaria , Adenosina/análogos & derivados , Adenosina/metabolismo , Metilación , Técnicas de Silenciamiento del Gen , Blastocisto/metabolismo , Embrión de Mamíferos/metabolismo , ARN Mensajero/metabolismo , ARN Mensajero/genéticaRESUMEN
Cell membrane-based nanovesicles (CMNVs) play pivotal roles in biomolecular transportation in living organisms and appear as attractive bioinformed nanomaterials for theranostic applications. However, the current surface-engineering technologies are limited in flexibility and orthogonality, making it challenging to simultaneously display multiple different ligands on the CMNV surface in a precisely controlled manner. Here, we developed a DNA scaffold-programmed approach to orthogonally engineer CMNVs with versatile ligands. The designed DNA scaffolds can rapidly anchor onto the CMNV surface, and their unique sequences and hybridized properties enable independent control of the loading of multiple different types of biomolecules on the CMNVs. As a result, the orthogonal engineering of CMNVs with a renal targeted peptide and a therapeutic protein at controlled ratios demonstrated an enhanced renal targeting and repair potential in vivo. This study highlights that a DNA scaffold-programmed platform can provide a potent means for orthogonal and flexible surface engineering of CMNVs for diverse therapeutic purposes.
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Silkworm pupae as widely consumed insect products are good biosources of protein and micronutrients. Silkworm rearing throughout the year can be achieved by feeding them an artificial diet instead of native plants, facilitating extensive pupa production. However, artificial diets are prone to spoilage caused by bacterial contamination. Here, we evaluated the antiseptic effect of ethylparaben (EP, chemical preservative) and medium-chain fatty acids (MCFA, natural preservative) in a silkworm artificial diet. Results showed that both preservatives effectively inhibited pathogenic bacterial growth. Furthermore, the addition of EP or MCFA did not negatively impact the production capacity of silkworms and the homeostasis of gut microbiota. However, the expression of genes involved in detoxification such as Ugt2, and immune response such as Cecropin B, were upregulated after EP consumption. Therefore, natural preservative MCFA emerges as a suitable option from a safety perspective. These findings highlight future directions for improving insect artificial diet formulation.
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In this paper we explore the application of low-loss multimode anti-resonant hollow-core fiber (MM-AR-HCF) in the delivery of nanosecond laser pulses at 1â µm wavelength. MM-AR-HCF with large core offers a rich content of low-loss higher-order modes which plays a key role in the efficient coupling and transmission of high-power laser of low beam quality. In the experiment, laser pulses of an average pulse energy of 21.8 mJ with 14.6â ns pulse width (corresponding a peak power of 1.49â MW) are transmitted through MM-AR-HCF of 9.8 m length without damage. 85% transmission efficiency is achieved where the incident laser beam suffers a low beam quality with M2 x and M2 y of 2.18 and 1.99 respectively. Laser-induced damage threshold (LIDT) of MM-AR-HCF was measured to be 22.6 mJ for 85% transmission efficiency, which is 7 times higher than that for a multimode silica optical fiber with a large core of 200â µm.
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Water buffalo Hunnivirus (BufHuV) belongs to the family Picornaviridae and is a newly discovered member of the Hunnivirus A genus. It causes intestinal diseases in cattle, mainly lead to subclinical infections, thereby seriously threatening the health of cattle herds. In addition, it can also bring about various clinical disease syndromes which results in severe economic losses to the cattle industry. To date, there have been no reports worldwide on the study of Hunnivirus virus infecting host cells and causing innate immune responses. In this study, we found that interferon treatment effectively blocked BufHuV replication and infection with the virus weakened the host antiviral responses. Inhibiting the transcription of IFN-ß and ISGs induced by either Sendai virus (SeV) or poly(I:C) in MDBK and HCT-8 cells, were dependent on the IRF3 or NF-κB signaling pathways, and this inhibited the activation of IFN-ß promoter by TBK1 and its upstream molecules, RIGI and MDA5. By constructing and screening five BufHuV proteins, we found that VP2, 2â¯C, 3â¯C and 3D inhibited the activation of IFN-ß promoter induced by SeV. Subsequently, we showed that VP2 inhibited the activation of IRF3 induced by SeV or poly (I:C), and it inhibited IRF3 activation by inhibiting its phosphorylation and nuclear translocation. In addition, we confirmed that VP2 inhibited the activation of IFNß induced by signaling molecules, MDA5 and TBKI. In summary, these findings provide new insights into the pathogenesis of Hunnivirus and its mechanisms involved in evading host immune responses.
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Factor 3 Regulador del Interferón , Interferón beta , Interferón beta/genética , Interferón beta/inmunología , Factor 3 Regulador del Interferón/metabolismo , Factor 3 Regulador del Interferón/genética , Animales , Humanos , Línea Celular , Transducción de Señal/efectos de los fármacos , Proteínas Estructurales Virales/genética , Proteínas Estructurales Virales/metabolismo , Replicación Viral/efectos de los fármacos , Inmunidad Innata , Bovinos , Búfalos/virología , FN-kappa B/metabolismoRESUMEN
Almond hull, a substantial byproduct comprising more than half of almond fresh weight, has recently gained attention due to its functionality and sustainability benefits. Despite heightened interest, information regarding its toxicity remains limited. In order to assess its genotoxic potential, we conducted Good Laboratory Practice-compliant in vitro and in vivo studies following Organization for Economic Co-operation and Development (OECD) guidelines. No evidence of toxicity or mutagenicity was observed in a bacterial reverse mutation assay using five tester strains, evaluating almond hull at concentrations up to 5 mg/plate, with or without metabolic activation. Almond hull did not induce chromosome structural damage in a chromosome aberration assay using Chinese hamster ovary cells, nor did it cause any spermatogonial chromosomal aberration in tested male BALB/c mice. To evaluate its ability to induce DNA damage in rodents, a combined micronucleus assay was conducted in KM mice of both sexes. Almond hull was administered at doses of 1250, 2500, and 5000 mg/kg/day via gavage once daily for 2 days. No adverse effects of almond hull were observed in the micronucleus assay. Our results indicate no evidence of the genotoxic potential of almond hull administered up to the maximum concentrations of 5 g/kg, as recommended by OECD guidelines.
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Microbial signatures have emerged as promising biomarkers for disease diagnostics and prognostics, yet their variability across different studies calls for a standardized approach to biomarker research. Therefore, we introduce xMarkerFinder, a four-stage computational framework for microbial biomarker identification with comprehensive validations from cross-cohort datasets, including differential signature identification, model construction, model validation and biomarker interpretation. xMarkerFinder enables the identification and validation of reproducible biomarkers for cross-cohort studies, along with the establishment of classification models and potential microbiome-induced mechanisms. Originally developed for gut microbiome research, xMarkerFinder's adaptable design makes it applicable to various microbial habitats and data types. Distinct from existing biomarker research tools that typically concentrate on a singular aspect, xMarkerFinder uniquely incorporates a sophisticated feature selection process, specifically designed to address the heterogeneity between different cohorts, extensive internal and external validations, and detailed specificity assessments. Execution time varies depending on the sample size, selected algorithm and computational resource. Accessible via GitHub ( https://github.com/tjcadd2020/xMarkerFinder ), xMarkerFinder supports users with diverse expertise levels through different execution options, including step-to-step scripts with detailed tutorials and frequently asked questions, a single-command execution script, a ready-to-use Docker image and a user-friendly web server ( https://www.biosino.org/xmarkerfinder ).
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Circular RNA (circRNA) is abundantly expressed in preimplantation embryos and embryonic stem cells in mice and humans. However, its function and mechanism in early development of mammalian embryos remain unclear. Here, we showed that circHIRA mediated miR-196b-5p to regulate porcine early embryonic development. We verified the circular feature of circHIRA by sanger sequencing, and proved the authenticity of circHIRA by enzyme digestion test. HIRA and circHIRA were expressed in porcine early embryos, and its expression levels significantly increased from 8-cell stage onwards and reached the maximum at the blastocyst stage. Functional studies revealed that circHIRA knockdown not only significantly reduced the developmental efficiency of embryos from 8-cell stage to blastocyst stage, but also impaired the blastocyst quality. Mechanistically, integrated analysis of miRNA prediction and gene expression showed that circHIRA knockdown significantly increased the expression of miR-196b-5p in porcine early embryos. Furthermore, miR-196b-5p inhibitor injection could rescue the early development of circHIRA knockdown embryos. Taken together, the findings reveal that circHIRA regulates porcine early embryonic development via inhibiting the expression of miR-196b-5p.
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Desarrollo Embrionario , Regulación del Desarrollo de la Expresión Génica , MicroARNs , ARN Circular , Animales , MicroARNs/genética , Desarrollo Embrionario/genética , Porcinos , ARN Circular/genética , Blastocisto/metabolismo , Técnicas de Silenciamiento del GenRESUMEN
Ovarian cancer is one of the most common gynecological malignant tumors with insidious onset, strong invasiveness, and poor prognosis. Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells.
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Proliferación Celular , Factores de Transcripción Forkhead , Glucólisis , Neoplasias Ováricas , Piruvato Deshidrogenasa Quinasa Acetil-Transferidora , Humanos , Neoplasias Ováricas/patología , Neoplasias Ováricas/metabolismo , Neoplasias Ováricas/genética , Femenino , Glucólisis/genética , Piruvato Deshidrogenasa Quinasa Acetil-Transferidora/metabolismo , Piruvato Deshidrogenasa Quinasa Acetil-Transferidora/genética , Factores de Transcripción Forkhead/metabolismo , Factores de Transcripción Forkhead/genética , Línea Celular Tumoral , Fosforilación , Animales , Proliferación Celular/genética , Ratones , Movimiento Celular/genética , Regulación Neoplásica de la Expresión Génica , Retroalimentación Fisiológica , Ratones Desnudos , PronósticoRESUMEN
The mixture of whole-plant soybean and whole-plant corn silage (WPSCS) is nutrient balanced and is also a promising roughage for ruminants. However, few studies have investigated the changes in bacterial community succession in WPSCS inoculated with homofermentative and heterofermentative lactic acid bacteria (LAB) and whether WPSCS inoculated with LAB can improve fermentation quality by reducing nutrient losses. This study investigated the effect of Lactobacillus plantarum (L. plantarum) or Lactobacillus buchneri (L. buchneri) on the fermentation quality, aerobic stability, and bacterial community of WPSCS. A 40:60 ratio of whole-plant soybean corn was inoculated without (CK) or with L. plantarum (LP), L. buchneri (LB), and a mixture of LP and LB (LPB), and fermented for 14, 28, and 56 days, followed by 7 days of aerobic exposure. The 56-day silage results indicated that the dry matter content of the LP and LB groups reached 37.36 and 36.67%, respectively, which was much greater than that of the CK group (36.05%). The pH values of the LP, LB, and LPB groups were significantly lower than those of the CK group (p < 0.05). The ammoniacal nitrogen content of LB was significantly lower than that of the other three groups (p < 0.05), and the ammoniacal nitrogen content of LP and LPB was significantly lower than that of CK (p < 0.05). The acetic acid content and aerobic stability of the LB group were significantly greater than those of the CK, LP, and LPB groups (p < 0.05). High-throughput sequencing revealed a dominant bacteria shift from Proteobacteria in fresh forage to Firmicutes in silage at the phylum level. Lactobacillus remained the dominant genus in all silage. Linear discriminant analysis effect size (LEFSe) analysis identified Lactobacillus as relatively abundant in LP-treated silage and Weissella in LB-treated groups. The results of KEGG pathway analysis of the 16S rRNA gene of the silage microbial flora showed that the abundance of genes related to amino acid metabolism in the LP, LB, and LPB groups was lower than that in the CK group (p < 0.05). In conclusion, LAB application can improve the fermentation quality and nutritional value of WPSCS by regulating the succession of microbial communities and metabolic pathways during ensiling. Concurrently, the LB inoculant showed the potential to improve the aerobic stability of WPSCS.
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Sorsby fundus dystrophy (SFD) is a rare autosomal dominant disorder with macular dystrophy and severe visual loss. Mutations in TIMP3 gene has been related to SFD with mechanisms unclear. We have successfully reprogrammed the peripheral blood mononuclear cells (PBMCs) from an SFD patient carrying c.484G>A mutation in TIMP3 gene to induced pluripotent stem cells (iPSCs) and characterized their pluripotency and genetic stability. This line may serve as a useful tool to explore the role of TIMP3 in SFD pathogenesis.
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Células Madre Pluripotentes Inducidas , Mutación , Inhibidor Tisular de Metaloproteinasa-3 , Femenino , Humanos , Masculino , Línea Celular , Células Madre Pluripotentes Inducidas/metabolismo , Degeneración Macular/genética , Degeneración Macular/patología , Inhibidor Tisular de Metaloproteinasa-3/genéticaRESUMEN
The anemia of inflammation (AI) is characterized by the presence of inflammation and abnormal elevation of hepcidin. Accumulating evidence has proved that Rocaglamide (RocA) was involved in inflammation regulation. Nevertheless, the role of RocA in AI, especially in iron metabolism, has not been investigated, and its underlying mechanism remains elusive. Here, we demonstrated that RocA dramatically suppressed the elevation of hepcidin and ferritin in LPS-treated mice cell line RAW264.7 and peritoneal macrophages. In vivo study showed that RocA can restrain the depletion of serum iron (SI) and transferrin (Tf) saturation caused by LPS. Further investigation showed that RocA suppressed the upregulation of hepcidin mRNA and downregulation of Fpn1 protein expression in the spleen and liver of LPS-treated mice. Mechanistically, this effect was attributed to RocA's ability to inhibit the IL-6/STAT3 pathway, resulting in the suppression of hepcidin mRNA and subsequent increase in Fpn1 and TfR1 expression in LPS-treated macrophages. Moreover, RocA inhibited the elevation of the cellular labile iron pool (LIP) and reactive oxygen species (ROS) induced by LPS in RAW264.7 cells. These findings reveal a pivotal mechanism underlying the roles of RocA in modulating iron homeostasis and also provide a candidate natural product on alleviating AI.
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Benzofuranos , Hepcidinas , Homeostasis , Interleucina-6 , Hierro , Animales , Ratones , Anemia/metabolismo , Anemia/genética , Anemia/tratamiento farmacológico , Anemia/patología , Proteínas de Transporte de Catión/genética , Proteínas de Transporte de Catión/metabolismo , Ferritinas/metabolismo , Ferritinas/genética , Regulación de la Expresión Génica/efectos de los fármacos , Hepcidinas/efectos de los fármacos , Hepcidinas/genética , Hepcidinas/metabolismo , Homeostasis/efectos de los fármacos , Inflamación/metabolismo , Inflamación/genética , Inflamación/patología , Interleucina-6/metabolismo , Interleucina-6/genética , Hierro/metabolismo , Lipopolisacáridos/farmacología , Hígado/metabolismo , Hígado/patología , Macrófagos/metabolismo , Macrófagos/efectos de los fármacos , Células RAW 264.7 , Especies Reactivas de Oxígeno/metabolismo , Receptores de Transferrina/metabolismo , Receptores de Transferrina/genética , Transducción de Señal/efectos de los fármacos , Factor de Transcripción STAT3/metabolismo , Factor de Transcripción STAT3/genética , Benzofuranos/farmacologíaRESUMEN
Retinitis pigmentosa (RP) is a group of genetically heterogeneous retinopathy resulting in irreversible loss of vision. Mutations in RAX2 gene has been related to RP with mechanisms unclear. Here, we generated a human induced pluripotent stem cell (iPSC) line from peripheral blood mononuclear cells of a RP patient carrying c.77C > T mutation in RAX2 gene. This cell line was induced by integration-free episomal vectors and validated for pluripotency and differentiation capacity, which may serve as a model to study the role of RAX2 in RP pathogenesis.
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Proteínas de Homeodominio , Células Madre Pluripotentes Inducidas , Mutación , Retinitis Pigmentosa , Humanos , Retinitis Pigmentosa/genética , Retinitis Pigmentosa/patología , Células Madre Pluripotentes Inducidas/metabolismo , Proteínas de Homeodominio/genética , Proteínas de Homeodominio/metabolismo , Línea Celular , Diferenciación Celular , Proteínas del Ojo/genética , Proteínas del Ojo/metabolismo , Masculino , Factores de TranscripciónRESUMEN
This study presents the development of an in-situ background-free Raman fiber probe, employing two customized double-cladding anti-resonant hollow-core fibers (AR-HCFs). The Raman background noise measured in the AR-HCF probe is lower than that of a conventional multi-mode silica fiber by two orders of magnitude. A plug-in device for fiber coupling optics was designed that was compatible with a commercially available confocal Raman microscope, enabling in-situ Raman detection. The numerical aperture (NA) of both AR-HCF claddings exceeds 0.2 substantially enhancing the collection efficiency of Raman signals at the distal end of the fiber probe. The performance of our Raman fiber probe is demonstrated by characterizing samples of acrylonitrile-butadiene-styrene (ABS) plastics, alumina ceramics, and ethylene glycol solution.
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Design and fabrication of integrated multifunctional probes with intrinsic catalytic and detection abilities is of great importance to simplify the operation in biosensing application with high sensitivity. Herein, dual-emitting lanthanide coordination polymers (Ln-CPs) were facilely prepared by self-assembly of guanine diphosphate (GDP), terephthalic acid (TA), Tb3+ and Cu2+ designated as Tb/Cu-GDP/TA CPs. The doped Cu2+ endowed CPs with obviously enhanced peroxidase mimicking activity compared with free Cu2+. In the presence of H2O2, the probe catalyzed the oxidation of TA generating a new blue fluorescent product, while the fluorescence of Tb3+ decreased simultaneously. Therefore, a new sensitive ratiometric fluorescent sensor for H2O2 has been developed with a good linear range from 0.01 to 300 µM and limit of 1.62 nM. Moreover, the proposed platform could be extended to GSH ratiometric assay in the presence of H2O2, and interestingly, the detection performance could be easily adjusted by adding different concentration of H2O2. This work will facilitate the development of luminescent nanoenzymes based on Ln-CPs to construct the simple ratiomatric sensing platform.
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Sepsis, defined as a life-threatening organ dysfunction, is associated with increased mortality in individuals with diabetes mellitus. In sepsis under diabetic conditions (SUDC), the superimposed inflammatory response and excessive production of reactive oxygen species (ROS) can cause severe damage to the kidney and liver, making it challenging to effectively repair multi-organ injury. In this study, we report the development of a DNA-based bifunctional nanomedicine, termed IL10-rDON, generated by assembling interleukin 10 (IL10) with rectangular DNA origami nanostructures (rDON) to address multi-organ dysfunction in SUDC. IL10-rDON was shown to predominantly accumulate in the kidney and liver of diabetic mice in vivo and effectively alleviate inflammatory responses through its anti-inflammatory IL10 component. In addition, the consumption of rDON itself significantly reduced excessive ROS in the liver and kidney. Serum and histological examinations further confirmed that IL10-rDON treatment could effectively improve liver and kidney function, as well as the survival of mice with SUDC. This study demonstrates an attractive antioxidant and anti-inflammatory nanomedicine for addressing acute liver and renal failure. The integration of rDON with therapeutic agents using DNA nanotechnology is a promising strategy for generating multifunctional nanomedicine to treat multi-organ dysfunction and other complicated diseases. STATEMENT OF SIGNIFICANCE: Sepsis under diabetic conditions (SUDC) leads to high mortality due to multiple organ failure such as acute liver and kidney injury. The anti-inflammatory cytokine interleukin 10 (IL10) holds great potential to treat SUDC, while disadvantages of IL-10 such as short half-life, non-specific distribution and lack of antioxidant activities limit its wide clinical applications. In this study, we developed a DNA-based, bifunctional nanomedicine (IL10-rDON) by assembling IL10 with rectangular DNA origami nanostructures (rDON). We found that IL10-rDON preferentially accumulated and sufficiently attenuated the increased levels of ROS and inflammation in the kidney and liver injury sites, and eventually improved the survival rate of mice with SUDC. Our finding provides new insights into the application of DNA-based nanomedicine in treating multi-organ failure.