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The properties of nanopipettes largely rely on the materials introduced onto their inner walls, which allow for a vast extension of their sensing capabilities. The challenge of simultaneously enhancing the sensitivity and selectivity of nanopipettes for pH sensing remains, hindering their practical applications. Herein, we report insulin-modified nanopipettes with excellent pH response performances, which were prepared by introducing insulin onto their inner walls via a two-step reaction involving silanization and amidation. The pH response intensity based on ion current rectification was significantly enhanced by approximately 4.29 times when utilizing insulin-modified nanopipettes compared with bare ones, demonstrating a linear response within the pH range of 2.50 to 7.80. In addition, insulin-modified nanopipettes featured good reversibility and selectivity. The modification processes were monitored using the I-V curves, and the relevant mechanisms were discussed. The effects of solution pH and insulin concentration on the modification results were investigated to achieve optimal insulin introduction. This study showed that the pH response behavior of nanopipettes can be greatly improved by introducing versatile molecules onto the inner walls, thereby contributing to the development and utilization of pH-responsive nanopipettes.
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Insulina , Concentração de Íons de Hidrogênio , Insulina/química , Técnicas Biossensoriais/métodos , Íons/químicaRESUMO
Perfluorooctanoic acid (PFOA), a persistent organic pollutant known for its chemical stability, is widely dispersed in the environment, posing significant health risks to mammals through various exposure routes such as ingestion, inhalation, and dermal contact. In this study, mice were exposed to PFOA (0, 0.2, 2â¯mg/L) through drinking water for 180 days to investigate its toxic effects on the colon. We identified differentially expressed genes through RNA sequencing and validated the impact of PFOA on the expression of these genes in colon tissue. Our findings revealed that long-term exposure to PFOA caused inflammatory bowel disease (IBD)-like damage to the mouse colon. We found PFOA could induce damage to the intestinal barrier. Inhibition of the Wnt signaling pathway following PFOA exposure results in impaired stem cell function in the colon of mice. Furthermore, PFOA activated the PPAR signaling pathway, disrupting cellular lipid metabolism in colon tissues. Additionally, PFOA induced inflammatory responses in colon tissue, facilitating NLR family, pyrin domain containing 3 (NLRP3) inflammasome activation and cell apoptosis. This study offers a thorough understanding of the mechanisms responsible for the damage to mouse colon tissue resulting from long-term exposure to PFOA.
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Caprilatos , Colo , Fluorocarbonos , Animais , Caprilatos/toxicidade , Fluorocarbonos/toxicidade , Colo/efeitos dos fármacos , Colo/patologia , Camundongos , Apoptose/efeitos dos fármacos , Camundongos Endogâmicos C57BL , Metabolismo dos Lipídeos/efeitos dos fármacos , Via de Sinalização Wnt/efeitos dos fármacos , Masculino , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Doenças Inflamatórias Intestinais/induzido quimicamente , Receptores Ativados por Proliferador de Peroxissomo/metabolismo , Receptores Ativados por Proliferador de Peroxissomo/genética , Inflamassomos/efeitos dos fármacosRESUMO
Baicalin is an active compound extracted from Scutellaria baicalensis with antioxidant and anti-inflammatory properties. Bone mesenchymal stem cells (BMSCs)-derived exosomes have shown promise for the treatment of hepatic ischemia-reperfusion (I/R) injury. This study aims to investigate the role of Baicalin-pretreated BMSCs-derived exosomes in hepatic I/R injury and its mechanisms. BMSCs were pretreated with or without Baicalin, and their exosomes (Ba-Exo and Exo) were collected and characterized. These exosomes were administered to mice via tail vein injection. Treatment with Exo and Ba-Exo significantly suppressed the elevation of ALT and AST induced by hepatic injury. Additionally, both Exo and Ba-Exo treatments resulted in a reduction in the liver weight-to-body weight ratio. RT-PCR results revealed a significant downregulation of pro-inflammatory cytokines with Exo and Ba-Exo treatment. Both Exo and Ba-Exo treatment improved the Th17/Treg cell imbalance induced by I/R and reduced hepatic injury. Additionally, exosomes were cocultured with normal liver cells, and the expression of fibroblast growth factor 21 (FGF21) in liver cells was elevated through Ba-Exo treatment. After treatment, the JAK2/STAT3 pathway was inhibited, and FOXO1 expression was upregulated. Finally, recombinant FGF21 was injected into mouse tail veins to assess its effects. Recombinant FGF21 injection further inhibited the JAK2/STAT3 pathway, increased FOXO1 expression, and improved the Th17/Treg cell imbalance. In conclusion, this study confirms the protective effects of Exo and Ba-Exo against hepatic I/R injury. Ba-Exo mitigates hepatic I/R injury, achieved through inducing FGF21 expression in liver cells, inhibiting the JAK2/STAT3 pathway, and activating FOXO1 expression. Therefore, baicalin pretreatment emerges as a promising strategy to enhance the therapeutic capability of BMSCs-derived exosomes for hepatic I/R.
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Exossomos , Fatores de Crescimento de Fibroblastos , Flavonoides , Células-Tronco Mesenquimais , Traumatismo por Reperfusão , Transdução de Sinais , Linfócitos T Reguladores , Células Th17 , Animais , Masculino , Camundongos , Exossomos/metabolismo , Exossomos/transplante , Fatores de Crescimento de Fibroblastos/metabolismo , Flavonoides/farmacologia , Janus Quinase 2/metabolismo , Fígado/efeitos dos fármacos , Fígado/patologia , Fígado/metabolismo , Células-Tronco Mesenquimais/metabolismo , Células-Tronco Mesenquimais/efeitos dos fármacos , Camundongos Endogâmicos C57BL , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/patologia , Traumatismo por Reperfusão/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fator de Transcrição STAT3/metabolismo , Linfócitos T Reguladores/efeitos dos fármacos , Linfócitos T Reguladores/imunologia , Células Th17/imunologia , Células Th17/efeitos dos fármacosRESUMO
Human mesenchymal stem cells (hMSCs) possess broad prospects in pre-clinical research. In vitro amplification of hMSCs requires appropriate medium to reach the number of seed cells with clinical significance. However, the uncertainty of the heterologous components of the traditional fetal bovine serum (FBS) culture medium has great safety risks. Moreover, existing commercial hMSCs medium is very expensive, therefore a safer and more optimal hMSCs medium is urgently needed. Accordingly, we developed five components adipose-derived hMSCs (hADMSCs) medium without xenogenic components, named E5 SFM. which is mainly composed of knockout serum replacement (KSR), and additionally four components such as fibroblast growth factor and transferrin. Here, we mainly compared the E5 SFM with traditional FBS-containing medium and a commercial medium by surface markers testing, proliferation assay as well as osteogenic, adipogenic and chondrogenic differentiation assessment. We demonstrated that hADMSCs cultured in the E5 SFM showed similar morphological characteristics and immunophenotypes to those in other media. Notably, cell proliferative capability was similar to that in the commercial medium, but higher than that in the FBS-containing medium and other media. Additionally, their capabilities of adipogenic and osteogenic differentiation were significantly higher than those of other media. Consequently, we concluded that the E5 SFM medium can not only effectively promote cell proliferation of hMSCs, but also has optimal differentiative capacity and clear and simple ingredients.
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Neoplasias dos Ductos Biliares , Colangiocarcinoma , Humanos , Colangiocarcinoma/radioterapia , Colangiocarcinoma/cirurgia , Ductos Biliares Intra-Hepáticos/cirurgia , Neoplasias dos Ductos Biliares/radioterapia , Neoplasias dos Ductos Biliares/cirurgia , Hepatectomia , Resultado do Tratamento , Estudos RetrospectivosRESUMO
BACKGROUND: Traumatic brain injury (TBI) is a leading cause of long-term disability in young adults and induces complex neuropathological processes. Cellular autonomous and intercellular changes during the subacute phase contribute substantially to the neuropathology of TBI. However, the underlying mechanisms remain elusive. In this study, we explored the dysregulated cellular signaling during the subacute phase of TBI. METHODS: Single-cell RNA-sequencing data (GSE160763) of TBI were analyzed to explore the cell-cell communication in the subacute phase of TBI. Upregulated neurotrophic factor signaling was validated in a mouse model of TBI. Primary cell cultures and cell lines were used as in vitro models to examine the potential mechanisms affecting signaling. RESULTS: Single-cell RNA-sequencing analysis revealed that microglia and astrocytes were the most affected cells during the subacute phase of TBI. Cell-cell communication analysis demonstrated that signaling mediated by the non-canonical neurotrophic factors midkine (MDK), pleiotrophin (PTN), and prosaposin (PSAP) in the microglia/astrocytes was upregulated in the subacute phase of TBI. Time-course profiling showed that MDK, PTN, and PSAP expression was primarily upregulated in the subacute phase of TBI, and astrocytes were the major source of MDK and PTN after TBI. In vitro studies revealed that the expression of MDK, PTN, and PSAP in astrocytes was enhanced by activated microglia. Moreover, MDK and PTN promoted the proliferation of neural progenitors derived from human-induced pluripotent stem cells (iPSCs) and neurite growth in iPSC-derived neurons, whereas PSAP exclusively stimulated neurite growth. CONCLUSION: The non-canonical neurotrophic factors MDK, PTN, and PSAP were upregulated in the subacute phase of TBI and played a crucial role in neuroregeneration.
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Lesões Encefálicas Traumáticas , Fatores de Crescimento Neural , Animais , Humanos , Camundongos , Lesões Encefálicas Traumáticas/genética , Lesões Encefálicas Traumáticas/metabolismo , Lesões Encefálicas Traumáticas/patologia , Citocinas/metabolismo , Fatores de Crescimento Neural/genética , Fatores de Crescimento Neural/metabolismo , Neurônios/metabolismo , RNA , Transdução de SinaisRESUMO
Hepatic carcinoma (HCC) is one of the most common malignant tumors worldwide, and the prognosis of HCC patients is often poor. Long-chain non-coding RNA (lncRNA) distal-less homeobox 6 antisense 1 (DLX6-AS1) has been shown to be involved in the pathogenesis of various cancers. This study aims to investigate the expression of DLX6-AS1 in HCC patients and its prognostic value. The serum DLX6-AS1 was quantified using a reverse transcription-polymerase chain reaction (RT-PCR) assay in both HCC patients and healthy individuals, and the correlation of DLX6-AS1 with clinicopathological features of HCC patients, as well as the diagnostic and prognostic value of DLX6-AS1 for HCC patients, were analyzed. The results showed that the expression of serum DLX6-AS1 in HCC patients was significantly higher than that of healthy individuals (P < 0.05), and DLX6-AS1 was related to tumor differentiation, pathological staging, and lymph node metastasis (all P < 0.05). Patients with high DLX6-AS1 expression showed significantly higher mortality than those with low DLX6-AS1 expression, and the DLX6-AS1 expression in dead patients was significantly higher than that in living patients. Furthermore, the AUC of DLX6-AS1 for poor prognosis of HCC patients was larger than 0.8. The univariate analysis revealed that the poor prognosis of HCC patients was related to pathological staging, lymph node metastasis, differentiation, and DLX6-AS1 expression (all P < 0.05), and the Cox multivariate analysis revealed that pathological staging, lymph node metastasis, differentiation, and DLX6-AS1 expression were independent risk factors for poor prognosis of HCC patients (all P < 0.05). These findings suggest that DLX6-AS1 may be a promising target for diagnosis, treatment, and prognosis prediction of HCC patients.
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To meet the global need for carbon neutrality, we must first understand the role of urban carbon metabolism. In this study, we developed a land-energy-carbon framework to model the spatial and temporal variation of carbon flows in Beijing from 1990 to 2018. Based on the changes in carbon sequestration and energy consumption, we used ecological network analysis to identify the critical paths for achieving carbon neutrality during land-use changes, thereby revealing possible decarbonization pathways to achieve carbon neutrality. By using GIS software, changes in the center of gravity for carbon flows were visualized in each period, and future urban construction scenarios were explored based on land-use policy. We found that the direct carbon emission peaked in 2010, mostly due to a growing area of transportation and industrial land. Total integrated flows through the network decreased at an average annual rate of 3.8%, and the change from cultivated land to the socioeconomic sectors and the paths between each socioeconomic component accounted for 29.5 and 31.7% of the integrated flows during the study period. The socioeconomic sectors as key nodes in the network should focus both on their scale expansion and on using cleaner energy to reduce carbon emissions. The center of gravity gradually moved southward, indicating that the new emission centers should seek a greener mixture of land use. Reducing carbon emission will strongly relied on transforming Beijing's energy consumption structure and increasing green areas to improve carbon sinks. Our results provide insights into carbon flow paths that must be modified by implementing land-use policies to reduce carbon emission and produce a more sustainable urban metabolism.
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Sequestro de Carbono , Carbono , Carbono/análise , Indústrias , Fenômenos Físicos , Meios de TransporteRESUMO
Based on a variant strain, we constructed a gE/gI/TK-deleted pseudorabies virus (PRV). A total of 18 female mice were randomized to a vaccination group to receive PRV XJ delgE/gI/TK, a vehicle group to receive Dulbecco's modified Eagle's medium, and a mock group to confirm the protection of PRV delgE/gI/TK on the central nervous system in mice. Subsequently, the vaccination and vehicle groups were infected with PRV XJ. The mice in the vehicle group showed more severe neurological symptoms and higher viral loads than those in the vaccination group. The exudation of Evans blue and the expression of tight junction protein showed no difference in all groups. HE staining showed vacuolar neuronal degeneration in the vehicle group brain, but no tissue lesions were observed in the vaccination group. TNF-α, IL-6, and synuclein were upregulated in the brain of mice in the vehicle group, while those were inhibited among mice in the vaccination group. IFN-ß, IFN-γ, ISG15, Mx1, and OAS1 showed no difference in the brain between the vaccination and vehicle groups. In addition, TNF-α and IL-6 were inhibited, and antiviral factors were increased in the intestine of the mice in the vaccination group compared to those in the vehicle group. Our study showed that PRV XJ delgE/gI/TK inhibited neurological damage and the inflammation of the intestine and brain induced by PRV and activated the innate immunity of the intestine.
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Senecavirus A (SVA) is a new type of virus related to swine vesicular disease, which results in enormous economic losses worldwide. At present, the host transcriptional responses to SVA infection, host-SVA interactions, and the mechanism of SVA in innate immune modulation are not well understood. This study explores the gene expression profiles of PK-15 cells at 0, 6, 12, 18, 24, 36 h SVA post-infection by RNA sequencing. Our analysis identified 61, 510, 1,584, 2,460, and 2,359 differentially expressed genes (DEGs) in the comparison groups S6 vs. Control, S12 vs. Control, S18 vs. Control, S24 vs. Control, S36 vs. Control, respectively. The reproducibility and repeatability of the results were validated by RT-qPCR, and all DEGs exhibited expression patterns consistent with the RNA-seq results. According to GO enrichment analysis and KEGG pathway analysis of DEGs in different periods after SVA infection, we found that SVA infection significantly modified the host cell gene-expression patterns and the host cells responded in highly specific manners, including response to signal reception and transmission, external biotic stimulus, response to the virus and host immune defense response. Notably, we observed the specific induction of type III interferon IFN-λ1 and IFN-λ3, which indicated that type III interferon plays an important antiviral function in PK-15 cells. Furthermore, our results showed that SVA might be recognized by RIG-I/MDA-5 receptors first after infecting PK-15 cells and then activates downstream IRF7-mediated signaling pathways, causing an increase in the expression of type III interferon. This study could provide important insights into the modulation of host metabolism during SVA infection and provide a strong theoretical basis for a better understanding of the pathogenic mechanism and immune escape mechanism of SVA.
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Hydrogen bonding interactions among poly vinyl alcohol (PVA), xanthan gum (XG) and acrylic acid (AA) molecules have been utilized to prepare an environment-friendly interpenetrating double-network hydrogel dust suppressant (PVA-XG-PAA/SDBS) with the aim of enhancing the poor mechanical performance of current hydrogel dust suppressants. A single factor test was used to determine the optimal formulation conditions for the PVA-XG-PAA/SDBS, and the viscosity, surface tension, compression strength, wind resistance, water retention and biodegradability of the samples were measured. The results showed that the hydrogel with optimal usage contained 1.5 g, 0.1 g, and 6 g of PVA, XG and AA, respectively and the optimal reaction temperature was 55 °C. Under the optimal conditions, the viscosity was 45 mPa s, the surface tension was 30 mN/m, the compression strength of the dust suppressant-solidified coal pillar reached 126 kPa, and the degradation rate at the 8th cycle (40 days) after being buried in soil was 34%. Compared with a conventional hydrogel dust suppressant, like poly acrylic acid (PAA), and the dust suppressant sodium dodecyl benzene sulfonate (SDBS), the PVA-XG-PAA/SDBS showed better water retention, wind erosion resistance, and dust-solidifying properties. On the basis of these remarkable properties, the PVA-XG-PAA/SDBS is applicable for dust prevention during coal mining, transport, and storage, which enhances the dust suppression efficiency obviously and has significant meaning to the sustainable development of the coal mining industry while protecting the environment.
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Hidrogéis , Álcool de Polivinil , Acrilatos , Poeira , Polissacarídeos BacterianosRESUMO
The present study aimed to investigate the protective effects of etomidate on hyperoxia-induced acute lung injury in mice, particularly on the nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. Fifty specific pathogen-free mice were randomly divided into the blank control, model, high oxygen exposure + low etomidate dose (0.3 mg·kg-1), a high oxygen exposure + moderate etomidate dose (3 mg·kg-1), and a high oxygen exposure + high etomidate dose (10 mg·kg-1) groups, with ten mice allotted per group. After 72 h, the mice were sacrificed and the lung tissues were harvested, and the wet-to-dry (W/D) ratio of the tissues was calculated. Hematoxylin-eosin staining was performed to observe the pathological changes in the lung tissues, and the lung injury score (LIS) was calculated. The mRNA and protein expression levels of Nrf2 and HO-1 were measured. The malondialdehyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT) levels were also measured, and interleukin (IL)-1ß, IL-6, tumor necrosis factor alpha (TNF-α) and IL-10 concentrations in the bronchoalveolar lavage fluid were determined. At low and moderate doses, etomidate decreased pathological damage in the lung tissue, decreased the LIS and W/D ratio, upregulated Nrf2 and HO-1 mRNA and protein expression, decreased IL-1ß, IL-6, and TNF-α concentrations, increased MPO activity and IL-10 levels, suppressed the production of the oxidation product MDA, and enhanced the activities of the antioxidant enzymes CAT and SOD. Within a certain dose range, etomidate enhanced antioxidant and anti-inflammatory effects in mice, thereby decreasing lung injury induced by the chronic inhalation of oxygen at high concentrations. Furthermore, the underlying mechanism may be associate with the upregulation of the Nrf2/HO-1 signaling pathway.
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Zinc finger protein 281 (ZNF281) has been characterized as a tumor suppressive lncRNA in glioma. The present study aimed to analyze the functionality of ZNF281 in osteosarcoma (OS). It was demonstrated that ZNF281 was downregulated in OS tissue specimens and predicted the survival of patients with OS. In tissues from patients with OS, ZNF281 was negatively associated with rho-associated coiled-coil containing protein kinase 1 (ROCK1), but positively associated with miR-144. In the U2OS cell line, ZNF281 overexpression mediated the upregulation of miR-44 and downregulation of ROCK1. miR-144 overexpression led to the downregulation of ROCK1, but failed to affect ZNF281. Expression of ZNF281 and miR-144 resulted in decreased cell migration and invasion, while ROCK1 overexpression resulted in increased invasion and migration of OS cells. In addition, ROCK1 overexpression attenuated the effects of ZNF281 and miR-144 overexpression. Thus, ZNF281 may downregulate ROCK1 by upregulating miR-144 and inhibit cancer cell invasion and migration in OS.
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Ischemic postconditioning provides robust neuroprotection, therefore, determining the molecular events may provide promising targets for stroke treatment. Here, we showed that the expression of functional mitochondrial voltage-dependent anion channel proteins (VDAC1, VDAC2, and VDAC3) reduced in rat vulnerable hippocampal CA1 subfield after global ischemia. Ischemic postconditioning restored VDACs to physiological levels. Stabilized VDACs contributed to the benefits of postconditioning. VDAC1 was required for maintaining neuronal Ca2+ buffering capacity. We found that microRNA-7 (miR-7) was responsible for postischemic decline of VDAC1 and VDAC3. Notably, miR-7 was more highly expressed in the peripheral blood of patients with acute ischemic stroke compared to healthy controls. Inhibition of miR-7 attenuated neuronal loss and ATP decline after global ischemia, but also diminished the infarct volume with improved neurological functions after focal ischemia. Thus, ischemic postconditioning protects against mitochondrial damage by stabilizing VDACs. MiR-7 may be a potential therapeutic target for ischemic stroke.
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Isquemia Encefálica/metabolismo , Neuroproteção/fisiologia , Canais de Ânion Dependentes de Voltagem/metabolismo , Animais , Pós-Condicionamento Isquêmico/métodos , Masculino , MicroRNAs/metabolismo , Mitocôndrias/metabolismo , Proteínas Mitocondriais/metabolismo , Ratos , Ratos Sprague-Dawley , Acidente Vascular Cerebral/metabolismoRESUMO
Tinnitus is thought to be caused by damage to the auditory and nonauditory system due to exposure to loud noise, aging, or other etiologies. However, at present, the exact neurophysiological basis of chronic tinnitus remains unknown. To explore whether the function of the limbic system is disturbed in tinnitus, the hippocampus was selected, which plays a vital role in learning and memory. The hippocampal function was examined with a learning and memory procedure. For this purpose, sodium salicylate (NaSal) was used to create a rat animal model of tinnitus, evaluated with prepulse inhibition behavior (PPI). The acquisition and retrieval abilities of spatial memory were measured using the Morris water maze (MWM) in NaSal-treated and control animals, followed by observation of c-Fos and delta-FosB protein expression in the hippocampal field by immunohistochemistry. To further identify the neural substrate for memory change in tinnitus, neurogenesis in the subgranular zone of the dentate gyrus (DG) was compared between the NaSal group and the control group. The results showed that acquisition and retrieval of spatial memory were impaired by NaSal treatment. The expression of c-Fos and delta-FosB protein was also inhibited in NaSal-treated animals. Simultaneously, neurogenesis in the DG was also impaired in tinnitus animals. In general, our data suggest that the hippocampal system (limbic system) may play a key role in tinnitus pathology.
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Hipocampo/efeitos dos fármacos , Aprendizagem em Labirinto/efeitos dos fármacos , Neurogênese/efeitos dos fármacos , Salicilato de Sódio/efeitos adversos , Memória Espacial/efeitos dos fármacos , Animais , Comportamento Animal , Modelos Animais de Doenças , Hipocampo/fisiologia , Masculino , Proteínas Proto-Oncogênicas c-fos/análise , Proteínas Proto-Oncogênicas c-fos/metabolismo , Ratos , Ratos Sprague-Dawley , Zumbido/induzido quimicamenteRESUMO
Cystic echinococcosis is a severe parasitic disease that commonly affects the liver and causes abscesses or rupture into the surrounding tissues, leading to multiple complications, such as shock, severe abdominal pain, and post-treatment abscess recurrence. Currently, there are no efficient measures to prevent these complications. We previously confirmed that arsenic trioxide (As2O3) exhibited in vitro cytotoxicity against Echinococcus granulosus protoscoleces. In the present study, we aimed to explore the mechanism of As2O3-induced E. granulosus protoscoleces apoptosis. After exposing E. granulosus protoscoleces to 0, 4, 6, and 8 µM As2O3, reactive oxygen species (ROS) level was detected by fluorescence microscopy; superoxide dismutase (SOD), and caspase-3 activities were measured; intracellular Ca2+ was detected by flow cytometry; GRP-78 and caspase-12 protein levels were measured by western blot analysis. Our results showed that the expression of caspase-3 was gradually increased and the expression of SOD was gradually decreased in As2O3-treated groups of protoscoleces. Simultaneously, fluorescence microscopy and flow cytometry showed that the ROS level and the intracellular Ca2+ level were increased in a time- and dose-dependent manner. Western blot analysis showed that the expressions of GRP-78 and caspase-12 were higher in As2O3-treated groups than in the control group. These results suggest that As2O3-induced apoptosis in E. granulosus protoscoleces is related to elevation of ROS level, disruption of intracellular Ca2+ homeostasis, and endoplasmic reticulum stress. These mechanisms can be targeted in the future by safer and more effective drugs to prevent recurrence of cystic echinococcosis.
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Apoptose/efeitos dos fármacos , Arsenicais/farmacologia , Cálcio/metabolismo , Echinococcus granulosus/efeitos dos fármacos , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Óxidos/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Animais , Trióxido de Arsênio , Caspase 12/metabolismo , Caspase 3/metabolismo , Equinococose/parasitologia , Echinococcus granulosus/metabolismo , Echinococcus granulosus/fisiologia , Chaperona BiP do Retículo Endoplasmático , Proteínas de Choque Térmico/metabolismo , Proteínas de Helminto/metabolismo , Ovinos , Doenças dos Ovinos/parasitologia , Superóxido Dismutase/metabolismoRESUMO
Vanadium is a trace element in the human body, and vanadium compounds have a promising future in biological and medical applications due to their various biological activities and low toxicity. Herein, a novel pure vanadium dioxide (VO2) nanofilm was deposited on a substrate of biomedical titanium by magnetron sputtering. The antibacterial effect of VO2 against the methicillin-resistant Staphylococcus aureus (MRSA) was validated in vitro and in vivo. Moreover, the biocompatibility of VO2 and its osteogenic effects were systematically illustrated. A possible osteogenic mechanism involving the amelioration of highly reactive oxygen species (ROS) levels were investigated. According to the results of our present and previous studies, the simultaneous antibacterial and osteogenic effects of VO2 are attributed to its differential regulation of ROS levels in rat bone marrow mesenchymal stem cells (rBMSCs) and bacteria. This study is the first to report the simultaneous effects of VO2 on bactericidal and osteogenic activities through its differential modification of ROS activity in eukaryotic (rBMSCs) and prokaryotic (MRSA) cells. The findings in this work may yield a deeper understanding of the biological activities of vanadium compounds while also paving the way for the further investigation and application of VO2 in biological and medical materials.