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OBJECT: To evaluate the effectiveness of selective bipolar plasmakinetic technology based on bladder irrigation fluid color on hemostasis in HoLEP surgwery METHODS: A total of 209 patients who underwent HoLEP surgery from October 2021 to July 2023 were included and divided into Hemostasis Management Group and control group. the color of the irrigation fluid was categorized into 5 levels and the bipolar plasmakinetic technology was applied when the color came to level 4 or up. The following was analyzed: postoperative use of balloon compression, blood loss, irrigation time, length of hospital stay, and the number of a second operation. RESULTS: Only 4 patients in Hemostasis Management Group required postoperative urinary catheter balloon compression, while there are 15 in the control group(p=0.03). The average irrigation time for patients in the HM Group with bipolar plasmakinetic hemostasis was 21.88±13.76 hours, compared to that in patients with catheter balloon compression(p=0.007). CONCLUSION: Based on the bladder irrigation color chart, the selective application of bipolar plasmakinetic hemostasis led to a significant reduction in the number of patients requiring postoperative bladder catheter balloon compression. Secondly, the irrigation time of patients who underwent bipolar plasmakinetic hemostasis also decreased.
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Cor , Irrigação Terapêutica , Humanos , Estudos Retrospectivos , Masculino , Pessoa de Meia-Idade , Idoso , Hiperplasia Prostática/cirurgia , Prostatectomia/métodos , Bexiga Urinária/cirurgia , Hemostasia Cirúrgica/métodos , Perda Sanguínea Cirúrgica/prevenção & controleRESUMO
Introduction: Obesity, mainly caused by excessive accumulation of visceral fat, excessive fat metabolism will cause hormone secretion imbalance and inflammation and other diseases. is extremely detrimental to human health. Although many treatments are available for obesity, most treatments fail to exert a radical effect or are associated with several side effects. Traditional Chinese medicine (TCM) for regulating the intestinal flora, lipid content and inflammation is considered effective. Based on previous studies, Artemisia capillaris, Astragalus propinquus, Phellodendron amurense, Salvia miltiorrhiza, Poria cocos, and Anemarrhena asphodeloides were selected to prepare an innovative herbal formula. Methods: TCM was characterized by UHPLC-Q-Orbitrap-MS. The anti-inflammatory and lipid-lowering effects of the TCM formula prepared were evaluated in a high-fat diet-fed obese mouse model. The effects of the TCM formula on the intestinal flora were also investigated. Results: Weights and insulin resistance, as well as inflammation, decreased in the mice after treatment. At the same time, lipid metabolism increased after the mice were gavaged with the TCM formula for 2 weeks. The intestinal motility of the drug administration group was enhanced, with partial restoration of the intestinal flora. Conclusion: In summary, our innovative Chinese herbal formula significantly reduced weight, reduced intestinal inflammation, improved intestinal motility, and improved lipid metabolism in obese mice. Furthermore, the innovative formula effectively prevented relevant obesity-induced metastatic diseases in the mice.
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Suffering from the formation of metal-ion dendrites and low storage capacity, MXene materials exhibit unsatisfactory performance in Li and Na storage. In this study, we demonstrate that the MXene V3C2Cl2 structure can induce uniform Li and Na deposition. This is achieved through coherent heterogeneous interface reconstruction and regulated ion tiling by halogen surface termination. The high lattice matching (91% and 99%) between MXenes and Li/Na, along with positive Cl terminal regulation, guides Li/Na ions to nucleate uniformly on the V3C2Cl2 MXene matrix and grow in a planar manner. Cl termination proves effective in regulating Li/Na ions due to its moderate adsorption and diffusion coefficients. Furthermore, upon adsorption onto the Cl-terminated V3C2Cl2 monolayer, Li4 and Na4 clusters undergo dissociation, favoring uniform adsorption over cluster adsorption. V3C2Cl2 MXenes exhibit impressive Li/Na storage capacities of 434.07 mA h g-1 for Li and 217.03 mA h g-1 for Na, surpassing the Li storage capacity of Ti3C2Cl2 by three-fold and the Na storage capacity of V2C by 1.4 times. This study highlights the regulatory role of Cl surface terminals in dendrite formation and Li/Na ion deposition, with potential applications to other metal-ion storage electrodes.
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Aims: Thioredoxin-interacting protein (TXNIP) is a crucial molecular promoter of oxidative stress and has been identified to be associated with cellular senescence. It is an important mediator of ß cell insulin secretion and has effects on ß cell mass. However, its role in ß cell senescence is unclear. The present study was designed to investigate the effects and mechanisms of TXNIP on the senescence and aging- and diet-related dysfunction of ß cells. Methods: Human pancreatic paraffin tissues and serum samples from different ages were collected to detect TXNIP expression. TXNIP-/- and C57BL/6J mice were fed either a normal chow diet (NCD) or a high-fat diet (HFD) until 5, 11, 14, or 20 months. The recapitulation experiment was conducted with TXNIP protein injection. MIN6 cells were transfected with LV-TXNIP and LV-siTXNIP. The biochemical indexes, ageing-related markers, cell cycle proteins, and pathways were examined both in vivo and in vitro. Results: TXNIP expression showed an age-related increase in ß cells and serum samples from humans. TXNIP significantly impaired glucose metabolism and insulin secretion in an age-dependent manner. TXNIP aggravated age-related and obesity-induced structural failure, oxidative stress, decreased proliferation, increased apoptosis in ß cells, and induced the cell cycle arrest. TXNIP interacted with p38 mitogen-activated protein kinase (p38MAPK) and modulated the p16/p21-CDK-Rb axis to accelerate ß cell senescence. Innovation and Conclusions: The present study demonstrated that TXNIP may exacerbate pancreatic ß cell senescence and age-related dysfunction by inducing cell cycle arrest through the p38-p16/p21-CDK-Rb pathway, in natural and pathological states. Antioxid. Redox Signal. 38, 480-495.
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Células Secretoras de Insulina , Camundongos , Animais , Humanos , Células Secretoras de Insulina/metabolismo , Camundongos Endogâmicos C57BL , Pontos de Checagem do Ciclo Celular , Senescência Celular , Proteínas de Ciclo Celular , Proteínas de Transporte/metabolismo , Tiorredoxinas/metabolismoRESUMO
Dried ginger is a commonly used stomachic. Dried ginger is often used as a gastric protector to treat stomach-related diseases. However, the effect of dried ginger on energy metabolism in stomach tissue of rats under physiological condition has not been studied. In this study, different doses of water extract of dried ginger were given to rats for 4â weeks. The activity of Na+ -K+ -ATPase, Ca2+ -Mg2+ -ATPase, SDH (succinate dehydrogenase) enzyme, ATP content, mitochondrial metabolic rate and mitochondrial number in stomach tissue of rats were measured. Analysis of potential biomarkers related to the effect of dried ginger on energy metabolism in stomach tissue of rats by metabonomics, and their metabolic pathways were also analyzed. The results revealed that there was no significant difference in Na+ -K+ -ATPase in high-dose group (GJH), medium-dose group (GJM) and low-dose group (GJL) compared to the Control group. The Ca2+ -Mg2+ -ATPase activity was significantly increased in stomach tissue of GJH group and GJM group, but there were no significant changes in stomach tissue of GJL group. The SDH activity and the ATP levels were significantly increased in stomach tissue of GJH group, GJM group and GJL group. The mitochondrial metabolic rate was significantly increased in GJL group, but there was no significant change in GJM group and was inhibited in GJH group. These effects might be mediated by arginine biosynthesis, glutathione metabolism, arachidonic acid metabolism, glycerophospholipid metabolism, arginine and proline metabolism, purine metabolism pathway.
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Metabolismo Energético , Zingiber officinale , Animais , Ratos , Adenosina Trifosfatases/metabolismo , Trifosfato de Adenosina/metabolismo , Arginina/metabolismo , Metabolismo Energético/efeitos dos fármacos , Zingiber officinale/química , Estômago/efeitos dos fármacos , Estômago/metabolismo , MetabolômicaRESUMO
Kidney ageing, which is always accompanied by renal fibrosis, drives the progression of renal fibrosis. Thioredoxin-interacting protein (TXNIP) is an endogenous suppressor of the reactive oxygen species-scavenging protein thioredoxin, which has been implicated in the ageing of some organs and is involved in renal fibrosis. However, the expression of TXNIP in ageing kidneys has not been examined, and the relationship between TXNIP and ageing-related renal fibrosis is unclear. We found that TXNIP expression was upregulated in aged mouse kidneys, and this upregulation was accompanied by ageing-related renal fibrosis phenotypes. We demonstrated that the ageing biomarkers were downregulated in TXNIP-knockout mice, and these effects resulted in the alleviation of renal fibrosis and impairments in kidney function. TXNIP overexpression in tubular cells upregulated senescence markers, promoted a profibrotic response and activated STAT3 signalling, and these parameters were inhibited by the silencing of TXNIP. Similarly, the TXNIP-mediated profibrotic response was significantly suppressed by a STAT3 inhibitor. By coimmunoprecipitation, we verified that TXNIP directly bound to STAT3, which suggested that TXNIP exacerbates renal tubular epithelial fibrosis by activating the STAT3 pathway. In summary, TXNIP plays an important role in age-related renal fibrosis and might be a therapeutic target for preventing ageing-associated renal fibrosis.
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Proteínas de Transporte/metabolismo , Rim , Fator de Transcrição STAT3/metabolismo , Tiorredoxinas/metabolismo , Animais , Células Cultivadas , Senescência Celular/fisiologia , Descoberta de Drogas , Fibrose/metabolismo , Fibrose/prevenção & controle , Perfilação da Expressão Gênica/métodos , Humanos , Rim/patologia , Rim/fisiologia , Rim/fisiopatologia , Camundongos , Camundongos Knockout , Estresse Oxidativo/efeitos dos fármacos , Fator de Transcrição STAT3/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacos , Regulação para CimaRESUMO
High-voltage lithium cobalt oxide (LCO) cathode material always suffers from rapid capacity decay due to irreversible phase transition and unexpected parasitic reactions between the charged LCO and conventional carbonate electrolyte. Here, a series of fluorinated electrolytes containing single or multiple fluorinated solvents were sought to match the high-voltage LCO cathode. The effects of regulating solvent components on the electrolyte properties, interfacial chemistry on both LCO cathode and mesocarbon microbead (MCMB) anode, and electrochemical performance of the LCO/MCMB cell were investigated. It is found that the synergistic effect of the fluorinated solvents obviously improves the reversible capacity and cycle capability for various half/full cell construction, in virtue of enhanced oxidation resistivity of the electrolyte and moderately-modified surface film on the cathode/anode. A novel perfluorinated electrolyte entirely consisting of fluorinated carbonate and fluorinated ether offers superior overall performance for the LCO/MCMB full cell at the upper cut-off voltage of 4.45 V.
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Thioredoxin-interacting protein (TXNIP) is a known important regulatory protein of islet ß-cell biology and function, but the detailed mechanism is not clear. Autophagy plays a pivotal role in maintaining cellular homoeostasis. This study aimed to elucidate the influence of TXNIP on the autophagy of ß-cell. In this study, C57BL/6 mice and TXNIP-/- mice were fed with a standard diet (SD) or a high-fat and high-sugar diet (HFSD), and then we analysed biochemical and autophagy related indexes in the mice. We infected MIN6 cells with LV-TXNIP and siRNA TXNIP, then the cells were treated with free fatty acid (FFA), autophagic activator rapamycin (RAP), inhibitors of autophagy chloroquine (CQ) and bafilomycin A1(BAF), finally, we examined the changes of autophagy in MIN6 cells. The results showed that HFSD led to ß-cell dysfunction and autophagy dysregulation, which was improved by TXNIP knockout in mice. In vitro experiments, TXNIP gene silencing enhanced LC3B-I conversion to LC3B-II, reduced the protein level of P62, decreased autophagosome accumulation induced by FFA treatment, increased the glucose-stimulated insulin secretion (GSIS) and autophagic flux inhibited by treatment with CQ. TXNIP overexpression induced upregulation of LC3B-I, LC3B-II and P62, accentuating the increase in autophagy and organelle destruction induced by FFA, and exacerbated the effect of BAF on the accumulation of autophagy proteins. Increasing TXNIP levels reduced GSIS, which was reversed by treatment with RAP. In summary, our study suggested that TXNIP is a critical link between autophagy disorders and pancreatic ß-cell dysfunction.
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Células Secretoras de Insulina , Ilhotas Pancreáticas , Animais , Autofagia , Proteínas de Transporte , Camundongos , Camundongos Endogâmicos C57BL , TiorredoxinasRESUMO
Objective To investigate the effect of thioredoxin interacting protein (TXNIP) over-expression on the apoptosis of MIN6 ß-cells and the mechanism involved. Methods Lentivirus carrying TXNIP gene was used to infect MIN6 ß-cells in logarithmic growth phase, and the infection efficiency was evaluated by fluorescence microscope and Western blotting. Then MIN6 ß-cells were divided into three groups: control group, empty lentivirus vector (LV-GFP) group and TXNIP over-expression (LV-GFP-TXNIP) group. CCK-8 assay was used to detect cell proliferation. AnnexinV-FITC/PI double staining was utilized to measure the apoptosis of MIN6 cells. Western blotting was applied to detect the expressions of TXNIP protein, TRX, Bax, Bcl2, cleaved caspase-3 (c-caspase-3), p38 mitogen-activated protein kinase (p38MAPK), phospho-p38MAPK (p-p38MAPK) proteins in the MIN6 ß-cells before and after treated with p38MAPK inhibitor SP169316. Results At 72 hours after the infection, the infection rate reached (87.10±2.30)% and (92.21±0.54)% in LV-GFP group and LV-GFP-TXNIP group, respectively, suggesting that lentivirus-mediated TXNIP over-expression was desirable. Compared with control group and LV-GFP group, the cell viability markedly decreased, and cell apoptosis, Bax/Bcl2 ratio, expression of c-caspased-3 and p38MAPK phosphorylation significantly increased in LV-GFP-TXNIP group. However, both the Bax/Bcl2 ratio and c-caspase-3 protein expression in LV-GFP-TXNIP group were obviously reduced after treated with p38MAPK inhibitor. Conclusion TXNIP over-expression might promote the apoptosis of MIN6 cells via activating the p38 MAPK pathway.
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Apoptose , Proteínas de Transporte/metabolismo , Transdução de Sinais , Tiorredoxinas/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Western Blotting , Proteínas de Transporte/genética , Caspase 3/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Insulinoma/genética , Insulinoma/metabolismo , Insulinoma/patologia , Camundongos , Microscopia de Fluorescência , Fosforilação , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Tiorredoxinas/genética , Proteína X Associada a bcl-2/metabolismoRESUMO
Protein arginine methyltransferase 1 (PRMT1) catalyzes methylation of histones and other cellular proteins, and thus regulates gene transcription and protein activity. In antigen-induced pulmonary inflammation (AIPI) PRMT1 was up-regulated in the epithelium, while in chronic AIPI, increased PRMT1 shifted to fibroblasts. In this study we investigated the cell type specific regulatory mechanism of PRMT1. Epithelial cells and fibroblasts were stimulated with IL-4 or IL-1ß. Gene and protein expression were determined by RT-qPCR, immunohistochemistry staining and Western blotting. Signaling pathway inhibitors, siRNAs and shRNA were used to determine the regulatory mechanism of PRMT1. The results showed that IL-4 up-regulated PRMT1 through STAT6 signaling in epithelial cells, while IL-1ß regulated PRMT1 through NF-κB in fibroblasts. The NF-kB inhibitor protein RKIP was highly expressed in epithelial cells and blocked IL-1ß induced PRMT1 up-regulation; while the STAT6 inhibitor protein PIAS1 was expressed in fibroblasts and suppressed IL-4 induced PRMT1 expression. Furthermore, IL-4 stimulated epithelial cells to release IL-1ß which up-regulated PRMT1 expression in fibroblasts. In conclusion, the inhibitor proteins RKIP and PIAS1 regulated the cell type and signaling specific expression of PRMT1. Thus PRMT1 expression in structural lung cells in asthma can be considered as potential target for new therapeutic intervention.
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Proteína de Ligação a Fosfatidiletanolamina/metabolismo , Proteínas Inibidoras de STAT Ativados/metabolismo , Proteína-Arginina N-Metiltransferases/metabolismo , Proteínas Repressoras/metabolismo , Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/metabolismo , Células A549 , Sítios de Ligação , Western Blotting , Células Cultivadas , Ciclo-Oxigenase 2/genética , Ciclo-Oxigenase 2/metabolismo , Células Epiteliais/citologia , Células Epiteliais/metabolismo , Fibroblastos/citologia , Fibroblastos/metabolismo , Humanos , Imunoprecipitação , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-1beta/farmacologia , Interleucina-4/genética , Interleucina-4/metabolismo , Interleucina-4/farmacologia , Pulmão/metabolismo , Pulmão/patologia , Microscopia de Fluorescência , NF-kappa B/antagonistas & inibidores , NF-kappa B/metabolismo , Proteína de Ligação a Fosfatidiletanolamina/antagonistas & inibidores , Proteína de Ligação a Fosfatidiletanolamina/genética , Fosforilação/efeitos dos fármacos , Pneumonia/metabolismo , Pneumonia/patologia , Regiões Promotoras Genéticas , Proteínas Inibidoras de STAT Ativados/antagonistas & inibidores , Proteínas Inibidoras de STAT Ativados/genética , Proteína-Arginina N-Metiltransferases/antagonistas & inibidores , Proteína-Arginina N-Metiltransferases/genética , Interferência de RNA , RNA Mensageiro/metabolismo , RNA Interferente Pequeno/metabolismo , Reação em Cadeia da Polimerase em Tempo Real , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/isolamento & purificação , Proteínas Recombinantes/farmacologia , Proteínas Repressoras/antagonistas & inibidores , Proteínas Repressoras/genética , Fator de Transcrição STAT6/antagonistas & inibidores , Fator de Transcrição STAT6/genética , Fator de Transcrição STAT6/metabolismo , Transdução de Sinais/efeitos dos fármacos , Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/antagonistas & inibidores , Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/genética , Regulação para Cima/efeitos dos fármacos , Fator A de Crescimento do Endotélio Vascular/genéticaRESUMO
Protein arginine methyltransferase (PRMT)1, methylating both histones and key cellular proteins, has emerged as a key regulator of various cellular processes. This study aimed to identify the mechanism that regulates PRMT1 in chronic Ag-induced pulmonary inflammation (AIPI) in the E3 rat asthma model. E3 rats were challenged with OVA for 1 or 8 wk to induce acute or chronic AIPI. Expression of mRNAs was detected by real-time quantitative PCR. PRMT1, TGF-ß, COX2, and vascular endothelial growth factor protein expression in lung tissues was determined by immunohistochemistry staining and Western blotting. In the in vitro study, IL-4-stimulated lung epithelial cell (A549) medium (ISEM) with or without anti-TGF-ß Ab was applied to human fibroblasts from lung (HFL1). The proliferation of HFL1 was determined by MTT. AMI-1 (pan-PRMT inhibitor) was administered intranasally to chronic AIPI rats to determine PRMT effects on asthmatic parameters. In lung tissue sections, PRMT1 expression was significantly upregulated, mainly in epithelial cells, in acute AIPI lungs, whereas it was significantly upregulated mainly in fibroblasts in chronic AIPI lungs. The in vitro study revealed that ISEM elevates PRMT1, COX2, and vascular endothelial growth factor expressions, and it promoted fibroblast proliferation. The application of anti-TGF-ß Ab suppressed COX2 upregulation by ISEM. AMI-1 inhibited the expression of COX2 in TGF-ß-stimulated cells. In the in vivo experiment, AMI-1 administered to AIPI rats reduced COX2 production and humoral immune response, and it abrogated mucus secretion and collagen generation. These findings suggested that TGF-ß-induced PRMT1 expression participates in fibroblast proliferation and chronic airway inflammation in AIPI.
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Asma/imunologia , Ciclo-Oxigenase 2/imunologia , Células Epiteliais/imunologia , Fibroblastos/imunologia , Proteína-Arginina N-Metiltransferases/imunologia , Fator de Crescimento Transformador beta/imunologia , Doença Aguda , Animais , Anticorpos/farmacologia , Asma/induzido quimicamente , Asma/genética , Asma/patologia , Proliferação de Células , Doença Crônica , Meios de Cultivo Condicionados/farmacologia , Ciclo-Oxigenase 2/genética , Inibidores Enzimáticos/farmacologia , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/patologia , Fibroblastos/efeitos dos fármacos , Fibroblastos/patologia , Regulação da Expressão Gênica , Humanos , Interleucina-4/farmacologia , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Pulmão/patologia , Naftalenossulfonatos/farmacologia , Ovalbumina , Pneumonia , Proteína-Arginina N-Metiltransferases/antagonistas & inibidores , Proteína-Arginina N-Metiltransferases/genética , Ratos , Transdução de Sinais , Fator de Crescimento Transformador beta/antagonistas & inibidores , Fator de Crescimento Transformador beta/genética , Ureia/análogos & derivados , Ureia/farmacologia , Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/imunologiaRESUMO
Pdcd4 has been known as a tumor-suppressor gene initially and is up-regulated during apoptosis. Surprisingly, we found that Pdcd4 was differentially expressed in the lung from E3 rats with AIPI, an animal model for asthma, but the precise role of Pdcd4 in AIPI still remained to be defined. In the present study, we first evaluated the expression of Pdcd4 in lung from control and AIPI rats with RT-qPCR, Western blot, and immunohistochemistry. Then, we investigated the effects of intervention of Pdcd4 on markers of macrophage alternative activation and airway remodeling. Upon challenging E3 rats with OVA, Pdcd4 was up-regulated in lung tissue with AIPI. Immunohistochemistry results showed that alveolar macrophages and airway epithelia expressed Pdcd4 protein. Overexpression of Pdcd4 in the rat alveolar macrophage cell line, NR8383 cells, increased the mRNA expression of arginase-1 and TGF-ß1, which are markers of macrophage alternative activation. In response to Pdcd4 RNAi in NR8383 cells, the mRNA expression of markers Fizz1, Ym1/2, arginase-1, and TGF-ß1 was decreased significantly. In addition, Pdcd4 RNAi in AIPI rats led to a decrease of the mRNA expression of Fizz1, Ym1/2, arginase-1, and TGF-ß1 in BALF cells. Finally, knockdown of Pdcd4 suppressed airway eosinophil infiltration, bronchus collagen deposition, and mucus production. Overall, these results suggest that Pdcd4 may be worthy of further investigation as a target for macrophage alternative activation and airway remodeling in allergic pulmonary inflammation.