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Li+ de-solvation at solid-electrolyte interphase (SEI)-electrolyte interface stands as a pivotal step that imposes limitations on the fast-charging capability and low-temperature performance of lithium-ion batteries (LIBs). Unraveling the contributions of key constituents in the SEI that facilitate Li+ de-solvation and deciphering their mechanisms, as a design principle for the interfacial structure of anode materials, is still a challenge. Herein, we conducted a systematic exploration of the influence exerted by various inorganic components (Li2CO3, LiF, Li3PO4) found in the SEI on their role in promoting the Li+ de-solvation. The findings highlight that Li3PO4-enriched SEI effectively reduces the de-solvation energy due to its ability to attenuate the Li+-solvent interaction, thereby expediting the de-solvation process. Building on this, we engineer Li3PO4 interphase on graphite (LPO-Gr) anode via a simple solid-phase coating, facilitating the Li+ de-solvation and building an inorganic-rich SEI, resulting in accelerated Li+ transport crossing the electrode interfaces and interphases. Full cells using the LPO-Gr anode can replenish its 80 % capacity in 6.5â minutes, while still retaining 70 % of the room temperature capacity even at -20 °C. Our strategy establishes connection between the de-solvation characteristics of the SEI components and the interfacial structure design of anode materials for high performance LIBs.
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Alloy anode materials have garnered unprecedented attention for potassium storage due to their high theoretical capacity. However, the substantial structural strain associated with deep potassiation results in serious electrode fragmentation and inadequate K-alloying reactions. Effectively reconciling the trade-off between low-strain and deep-potassiation in alloy anodes poses a considerable challenge due to the larger size of K-ions compared to Li/Na-ions. In this study, we propose a chemical bonding modulation strategy through single-atom modification to address the volume expansion of alloy anodes during potassiation. Using black phosphorus (BP) as a representative and generalizing to other alloy anodes, we established a robust P-S covalent bonding network via sulfur doping. This network exhibits sustained stability across discharge-charge cycles, elevating the modulus of K-P compounds by 74%, effectively withstanding the high strain induced by the potassiation process. Additionally, the bonding modulation reduces the formation energies of potassium phosphides, facilitating a deeper potassiation of the BP anode. As a result, the modified BP anode exhibits a high reversible capacity and extended operational lifespan, coupled with a high areal capacity. This work introduces a new perspective on overcoming the trade-off between low-strain and deep-potassiation in alloy anodes for the development of high-energy and stable potassium-ion batteries.
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Triptolide (TP) is a remarkable anti-inflammatory and immunosuppressive component separated from Tripterygium wilfordii Hook. F. However, its hepatotoxicity limits its application in the clinical. Our group has proposed a new perspective on TP-induced hepatotoxicity, in which TP enhances liver hypersensitivity upon lipopolysaccharide (LPS) stimulation. Because the cause of the disease is unknown, there is currently no uniform treatment available. In this study, we attempted to determine whether the GSK-3ß-JNK pathway affects liver damage and its regulatory mechanism in response to TP/LPS costimulation. In addition, we investigated the effect of CsA or the GSK 3ß inhibitor CHIR-98014 on TP/LPS-induced hepatotoxicity. The results showed that the TP/LPS cotreatment mice exhibited obvious hepatotoxicity, as indicated by a remarkable increase in the serum ALT and AST levels, glycogen depletion, GSK 3ß-JNK upregulation, and increased apoptosis. Instead of the specific knockdown of JNK1, the specific knockdown of JNK2 had a protective effect. Additionally, 40 mg/kg of CsA and 30 mg/kg of CHIR-98014 might provide protection. In summary, CHIR-98014 could protect against TP/LPS- or TP/TNF-α-induced activation of the GSK 3ß-JNK pathway and mitochondria-dependent apoptosis, improving the indirect hepatotoxicity induced by TP.
Asunto(s)
Aminopiridinas , Enfermedad Hepática Inducida por Sustancias y Drogas , Diterpenos , Fenantrenos , Pirimidinas , Ratones , Animales , Glucógeno Sintasa Quinasa 3 beta/farmacología , Lipopolisacáridos/toxicidad , Mitocondrias , Apoptosis , Diterpenos/farmacología , Fenantrenos/farmacología , Compuestos Epoxi/toxicidad , Enfermedad Hepática Inducida por Sustancias y Drogas/prevención & controlRESUMEN
The most successful lithium-ion batteries (LIBs) based on ethylene carbonate electrolytes and graphite anodes still suffer from severe energy and power loss at temperatures below -20 °C, which is because of high viscosity or even solidification of electrolytes, sluggish de-solvation of Li+ at the electrode surface, and slow Li+ transportation in solid electrolyte interphase (SEI). Here, a coherent lithium phosphide (Li3P) coating firmly bonding to the graphite surface to effectively address these challenges is engineered. The dense, continuous, and robust Li3P interphase with high ionic conductivity enhances Li+ transportation across the SEI. Plus, it promotes Li+ de-solvation through an electron transfer mechanism, which simultaneously accelerates the charge transport kinetics and stands against the co-intercalation of low-melting-point solvent molecules, such as propylene carbonate (PC), 1,3-dioxolane, and 1,2-dimethoxyethane. Consequently, an unprecedented combination of high-capacity retention and fast-charging ability for LIBs at low temperatures is achieved. In full-cells encompassing the Li3P-coated graphite anode and PC electrolytes, an impressive 70% of their room-temperature capacity is attained at -20 °C with a 4 C charging rate and a 65% capacity retention is achieved at -40 °C with a 0.05 C charging rate. This research pioneers a transformative trajectory in fortifying LIB performance in cryogenic environments.
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BACKGROUND: Mitochondria are multifunctional organelles, which participate in biochemical processes. Mitochondria act as primary energy producers and biosynthetic centers of cells, which are involved in oxidative stress responses and cell signaling transduction. Among numerous potential mechanisms of mitochondrial dysfunction, the opening of the mitochondrial permeability transition pore (mPTP) is a major determinant of mitochondrial dysfunction to induce cellular damage or death. A plenty of studies have provided evidence that the abnormal opening of mPTP induces the loss of mitochondrial membrane potential, the impairment calcium homeostasis and the decrease of ATP production. Cyclophilin D (CypD), localized in the mitochondrial transition pore, is a mitochondrial chaperone that has been regarded as a prominent mediator of mPTP. METHODS: This review describes the relationship between CypD, mPTP, and CypD-mPTP inhibitors through systematic investigation of recent relevant literature. RESULTS: Here, we have highlighted that inhibiting the activity of CypD protects models of some diseases, including ischaemia/reperfusion injury (IRI), neurodegenerative disorders and so on. Knockdown studies have demonstrated that CypD possibly is mediated by its peptidyl-prolyl cis-trans isomerase activity, while the primary targets of CypD remain obscure. The target of CypD-mPTP inhibitor can alleviate mPTP opening-induced cell death. The present review is focused on the role of CypD as a prominent mediator of the mPTP, further providing insight into the physiological function of mPTP and its regulation by CypD. CONCLUSION: Blocking the opening of mPTP by inhibiting CypD might be a new promising approach for suppressing cell death, which will suggest novel therapeutic approaches for mitochondria-related diseases.
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Proteínas de Transporte de Membrana Mitocondrial , Necrosis por Permeabilidad de la Transmembrana Mitocondrial , Peptidil-Prolil Isomerasa F , Humanos , Peptidil-Prolil Isomerasa F/metabolismo , Mitocondrias/metabolismo , Proteínas de Transporte de Membrana Mitocondrial/metabolismo , Poro de Transición de la Permeabilidad Mitocondrial/metabolismoRESUMEN
In view of their high lithium storage capability, phosphorus-based anodes are promising for lithium-ion batteries. However, the low reduction potential (0.74 V versus Li+ /Li) of the commonly used ethylene carbonate-based electrolyte does not allow the early formation of a solid electrolyte interphase (SEI) prior to the initial phosphorus alloying reaction (1.5 V versus Li+ /Li). In the absence of a protective SEI, the phosphorus anode develops cracks, creating additional P/electrolyte interfaces. This results in the loss of P and the formation of a discontinuous SEI, all of which greatly reduce the electrochemical performance of the anode. Here, the effect of solvent reduction potential on the structure of the SEI is investigated. It is found that solvents with a high reduction potential, such as fluoroethylene carbonate, decompose to form an SEI concomitantly with the P alloying reaction. This results in a continuous, mechanically robust, and Li3 PO4 -rich SEI with improved Li-ion conductivity. These attributes significantly improve the cyclic stability and rate performance of the phosphorus-based anode.
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This study was designed to investigate the potential role of farnesoid X receptor (FXR) in abnormal bile acid metabolism and pyroptosis during the pathogenesis of triptolide (TP)/lipopolysaccharide (LPS)-induced hepatotoxicity. Moreover, the protective effect of obeticholic acid (OCA) was explored under this condition. In vivo, female C57BL/6 mice were administrated with OCA (40 mg/kg bw, intragastrical injection) before (500 µg/kg bw, intragastrical injection)/LPS (0.1 mg/kg bw, intraperitoneal injection) administration. In vitro, AML12 cells were treated with TP (50 nM) and TNF-α (50 ng/ml) to induce hepatotoxicity; GW4064 (5 µM) and cholestyramine (CHO) (0.1 mg/ml and 0.05 mg/ml) were introduced to explain the role of FXR/total bile acid (TBA) in it. Serum TBA level was significantly elevated, which was induced by FXR suppression. And both GW4064 and CHO intervention presented remarkable protective effects against TP/TNF-α-induced NLRP3 upregulation and pyroptosis pathway activation. Pre-administration of FXR agonist OCA successfully attenuated TP/LPS-induced severe liver injury by reducing serum bile acids accumulation and inhibiting the activation of caspase-11-GSDMD (gasdermin D) pyroptosis pathway. We have drawn conclusions that TP aggravated liver hypersensitivity to LPS and inhibited FXR-SHP (small heterodimer partner) axis, which was served as endogenous signals to activate caspase-11-GSDMD-mediated pyroptosis contributing to liver injury. OCA alleviated TP/LPS-induced liver injury accompanied by inhibiting caspase-11-GSDMD-mediated pyroptosis pathway and decreased serum TBA level. The results indicated that FXR might be an attractive therapeutic target for TP/LPS-induced hepatotoxicity, providing an effective strategy for drug-induced liver injury.
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Enfermedad Hepática Inducida por Sustancias y Drogas , Lipopolisacáridos , Animales , Ratones , Femenino , Lipopolisacáridos/toxicidad , Piroptosis , Caspasas , Factor de Necrosis Tumoral alfa , Ratones Endogámicos C57BL , Ácidos y Sales Biliares , Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Enfermedad Hepática Inducida por Sustancias y Drogas/prevención & controlRESUMEN
Crumb rubber modified bitumen (CRMB) has excellent high-temperature performance and fatigue resistance, and is widely used in asphalt pavement to cope with increasing traffic axle load and changing climate. Under conventional preparation conditions, the swelling degree of CR can directly impact the comprehensive properties of CRMB; however, physical and chemical properties research on swelling crumb rubber (SCR) and crumb rubber recycled bitumen (CRRB) in CRMB is relatively lacking. In this paper, the working performance of CRMB and CRRB in high-temperature and low-temperature conditions were studied through physical and working performance testing of bitumen. The CR and SCR were tested by scanning electron microscope (SEM), Fourier transform infrared spectrometer (FTIR), gel permeation chromatography (GPC), and particle size distribution (PSD) tests to study the physicochemical behavior and microscopic effects before and after CR swelling. The results showed that CR dosage was in the range of 10%, 15%, and 20%, as well as that CR dosages have a positive effect on the high- and low-temperature performance, storage stability, and elastic recovery of bitumen. The high-temperature PG grades of bitumen were directly improved by four grades, and the elastic recovery rate increased by 339.9%. CR improved the ultra-low temperature crack resistance of bitumen. Due to the absorption of lighter components by CR, the relative content of the heavy component of bitumen increased; however, its low-temperature performance decreased significantly. After swelling, the CR particle size increased and the range became wider, the surface complexity of CR became higher, and the specific surface area was larger. At the same time, CR carried out the transformation process from large and medium molecules to small molecules. During the swelling process, a new benzene ring structure appeared in the CR, and the C-C bond and C-S bond of CR broke, forming part of the C=C bond.
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ETHNOPHARMACOLOGICAL RELEVANCE: Triptolide (TP) is a major active ingredient and toxic component of Tripterygium wilfordii Hook F (TWHF), which exhibits multiple activities and remarkable hepatotoxicity, the latter of which limits its clinical application due to the risk of liver injury. Previous research has revealed the hepatotoxicity of TP resulting in liver hypersensitivity upon lipopolysaccharide (LPS) stimulation. However, existing research has not elucidated the potential immune mechanism such as Th17/Treg imbalance in TP-induced hepatic excessive immune response to exogenous LPS. AIM OF THE STUDY: To investigate the role of Th17/Treg imbalance in TP-induced hepatic excessive immune response to exogenous LPS. MATERIALS AND METHODS: Mice were administered with TP, LPS, neutralization antibody and small molecule inhibitor respectively. Serum transaminase level was measured to determine the severity of liver injury. Frequencies of liver Th17 and Treg cells were analyzed by flow cytometry. Serum cytokine levels were performed by ELSIA, and mRNA levels of liver cytokine were performed by qPCR. The status of neutrophil infiltration was performed by myeloperoxidase (MPO) IHC measurement. Morphological observation of liver was performed by hematoxylin and eosin (H&E) staining. RESULTS: Mice given a single intragastric dose of TP (500 µg/kg) developed lethal fulminant hepatitis following intraperitoneal injection of LPS (0.1 mg/kg), characterized by low survival rate, severe liver injury, high levels of inflammation and neutrophil infiltration. Hepatic Th17/Treg imbalance emerged together with liver injury in these mice. Neutralization of IL-17A attenuated the liver injury and ameliorated the neutrophil infiltration. The TP-induced alteration of hepatic Th17/Treg balance was closely related to the outcome of immune-mediated acute liver injury triggered by LPS. Pretreatment with the STAT3 inhibitor AG490 effectively restored Th17/Treg balance, significantly reducing the production of IL-17A and finally attenuating the degree of liver injury. CONCLUSION: Hepatic Th17/Treg imbalance not only exacerbates TP- and LPS-induced liver injury, but also serves as an indispensable part in the mechanisms of TP-induced hepatic intolerance to exogenous endotoxin.
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Enfermedad Hepática Inducida por Sustancias y Drogas , Linfocitos T Reguladores , Animales , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Citocinas/genética , Citocinas/farmacología , Diterpenos , Compuestos Epoxi , Inmunidad , Interleucina-17 , Lipopolisacáridos/toxicidad , Ratones , Ratones Endogámicos C57BL , Fenantrenos , Células Th17RESUMEN
Headspace solid-phase microextraction (HS-SPME) technique was employed to extract the volatile components from Chinese traditional medicine, Atractlodes macrocephala Koidz. The volatile components were isolated and identified successfully by gas chromatography-mass spectrometry (GC-MS). The results from HS-SPME-GC-MS were compared with those obtained from steam distillation-GC-MS (SD-GC-MS) with a good agreement. The volatiles were collected using a polydimethylsiloxane-divinylbenzene (PDMS-DVB) fiber by HS-SPME. The best response was obtained when the extraction temperature was 70 degrees C, the equilibrium time and extraction time were all 30 min and the desorption time was 4 min. Analysis was performed by GC-MS with a polysiloxane capillary column (30 m x 0.25 mm, film thickness 0.25 microm) using He as the carrier gas and a programmed temperature run. Forty-one components accounting for 90.81% were identified. The main components (relative amount more than 1%) of the samples by HS-SPME were atractylone (40.12%), gamma-elemene (14.73%), aromadendrene (13.05%), eudesma-4 (14), 11-diene (5.46%), caryophyllene (2.56%), patchoulene (2.55%), 6,10,11,11-tetramethyl-tricyclo [6.3.0.1(2,3)] undec-7-ene (2.11%), cedrene (1.48%), alpha-caryophyllene (1.48%) and selina-4 (14) -7 (11) diene-8-one (1.01%). By SD-GC-MS, 31 components accounting for 88.19% were identified and all these components could be extracted by SPME except trans-beta-ocimene which accounts only 0.10%. The results showed that the HS-SPME technique can be used to extract the the volatile components from Atractlodes macrocephala Koidz. in place of the traditional time-consuming SD.