Publications by authors named "Junxian Hu"

10 Publications

  • Page 1 of 1

Stabilizing Na metal anode with NaF interface on spent cathode carbon from aluminum electrolysis.

Chem Commun (Camb) 2021 Jul 12. Epub 2021 Jul 12.

School of Metallurgy and Environment, Engineering Research Center of the Ministry of Education for Advanced Battery Materials, Hunan Provincial Key Laboratory of Nonferrous Value-Added Metallurgy, Central South University, Changsha, 410083, P. R. China.

We report the synthesis of spent cathode carbon (SCC) with a NaF interface from aluminum electrolysis, and its application as a Na metal anode host. The SCC anode exhibits superior ion conductivity and a high shear modulus. The natural NaF interface on the SCC anode can regulate Na+ transmission and inhibit dendrite growth. Furthermore, the anode can be used to turn waste into treasure through directly using spent cathodic carbon without any chemical processing. The green SCC electrode exhibits a higher flat voltage and better reversibility compared with purified cathode carbon without NaF.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/d1cc02654bDOI Listing
July 2021

Light rare earth elements hinder bone development via inhibiting type H vessels formation in mice.

Ecotoxicol Environ Saf 2021 May 4;218:112275. Epub 2021 May 4.

Department of Orthopedics, Southwest Hospital, Third Military Medical University, Army Medical University, Chongqing 400038, China. Electronic address:

Light rare earth elements (LREEs) are widely used in medical, industrial, and agricultural fields. Wide application of light rare earth and exposure to these elements in human society leads to increasing accumulation of LREE in human skeletal system. However, the effects of LREEs on human bone health is not clear. In this study, we found that LREE reduced CD31Emcn endothelial cell mediated type H vessels formation at the metaphyseal sites, resulting in reduced bone mass and low bone quality in mouse bone development. To explore the underlying mechanism, we induced bone marrow macrophages (BMMs) to preosteoclasts (pOCs) with exposure of LREE (Pr, Nd, Sm). The cytotoxicity of LREE was evaluated by CCK-8. Platelet-derived growth factor (PDGF-BB) is the cytokine secreted by pOCs that most responsible for inducing Type H vessel formation. We used ELISA kit to determine the PDGF-BB level in pOC supernatant, and mouse serum finding that the PDGF-BB level was reduced by LREEs treatment. Then we tested the ability of migration and tube formation of HUVECs using condition medium from pOCs. The migration and tube formation ability of HUVECs were both suppressed with LREEs pretreatment. We concluded that LREEs hinder mouse bone development by suppressing type H vessels associated bone formation. DATA AND MATERIALS AVAILABILITY: All data generated or analyzed during this study are included in this article. Please contact the corresponding author for unique material requests. Some material used in the reported research may require requests to collaborators and agreements with both commercial and non-profit institutions, as specified in the paper. Requests are reviewed by Third Military Medical University to verify whether the request is subject to any intellectual property or confidentiality obligations. Any material that can be shared will be released via a Material Transfer Agreement.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ecoenv.2021.112275DOI Listing
May 2021

Ferulic acid positively modulates the inflammatory response to septic liver injury through the GSK-3β/NF-κB/CREB pathway.

Life Sci 2021 Jul 4;277:119584. Epub 2021 May 4.

Department of Emergency Medicine, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, PR China. Electronic address:

Aims: Ferulic acid (FA) is a component found in plants that has free radical scavenging and liver-protective properties. Acute liver injury (ALI) is a serious complication of sepsis and is closely associated with changes in the levels of inflammatory factors. This study was taken to examine the role of FA in cecal ligation and perforation (CLP)-induced murine ALI and lipopolysaccharide (LPS)-induced cellular ALI models.

Materials And Methods: An in vivo ALI model was established by performing CLP surgery on C57BL/6 mice. After the ALI model was established, mice were examined for liver injury, including HE staining to observe tissue sections, the percentage of liver/body weight and inflammatory factor levels. Myeloperoxidase (MPO), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were measured in liver or serum using commercial kits. An in vitro ALI model was established using LPS-stimulated RAW264.7 cells. Cell viability was measured by MTT method and the intracellular levels of IL-10, IL-1β, IL-6, IL-12 and TNF-α inflammatory factors were measured using kits. The expression of GSK-3β, NF-κB and CREB was measured by western blot or immunofluorescence.

Key Findings: FA pretreatment significantly reduced liver/body weight ratio, decreased MPO, AST and ALT activity, alleviated the inflammatory responses and improved CLP-induced histopathological changes in liver. In addition, in vitro results showed that FA could dose-dependently increase the viability of RAW264.7 cells and decrease the levels of pro-inflammatory factors.

Significance: In conclusion, our data suggest that FA can ameliorate ALI-induced inflammation via the GSK-3β/NF-κB/CREB pathway, suggesting that FA can be used to protect the liver against ALI.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.lfs.2021.119584DOI Listing
July 2021

The effect of the WKYMVm peptide on promoting mBMSC secretion of exosomes to induce M2 macrophage polarization through the FPR2 pathway.

J Orthop Surg Res 2021 Mar 3;16(1):171. Epub 2021 Mar 3.

Department of Orthopedics, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.

Background: When multicystic vesicles (precursors of exosomes) are formed in cells, there are two results. One is decomposition by lysosomes, and the other is the generation of exosomes that are transported out through the transmembrane. On the other hand, M2 macrophages promote the formation of local vascularization and provide necessary support for the repair of bone defects. To provide a new idea for the treatment of bone defects, the purpose of our study was to investigate the effect of WKYMVm (Trp-Lys-Tyr-Met-Val-D-Met-NH2) peptide on the secretion of exosomes from murine bone marrow-derived MSCs (mBMSCs) and the effect of exosomes on the polarization of M2 macrophages.

Methods: The WKYMVm peptide was used to activate the formyl peptide receptor 2 (FPR2) pathway in mBMSCs. First, we used Cell Counting Kit-8 (CCK-8) to detect the cytotoxic effect of WKYMVm peptide on mBMSCs. Second, we used western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR) to detect the expression of interferon stimulated gene 15 (ISG15) and transcription factor EB (TFEB) in mBMSCs. Then, we detected lysosomal activity using a lysozyme activity assay kit. Third, we used an exosome extraction kit and western blotting to detect the content of exosomes secreted by mBMSCs. Fourth, we used immunofluorescence and western blotting to count the number of polarized M2 macrophages. Finally, we used an inhibitor to block miRNA-146 in exosomes secreted by mBMSCs and counted the number of polarized M2 macrophages.

Results: We first found that the WKYMVm peptide had no toxic effect on mBMSCs at a concentration of 1 μmol/L. Second, we found that when the FPR2 pathway was activated by the WKYMVm peptide in mBMSCs, ISG15 and TFEB expression was decreased, leading to increased secretion of exosomes. We also found that lysosomal activity was decreased when the FPR2 pathway was activated by the WKYMVm peptide in mBMSCs. Third, we demonstrated that exosomes secreted by mBMSCs promote the polarization of M2 macrophages. Moreover, all these effects can be blocked by the WRWWWW (WRW4, H-Trp-Arg-Trp-Trp-Trp-Trp-OH) peptide, an inhibitor of the FPR2 pathway. Finally, we confirmed the effect of miRNA-146 in exosomes secreted by mBMSCs on promoting the polarization of M2 macrophages.

Conclusion: Our findings demonstrated the potential value of the WKYMVm peptide in promoting the secretion of exosomes by mBMSCs and eventually leading to M2 macrophage polarization. We believe that our study could provide a research basis for the clinical treatment of bone defects.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s13018-021-02321-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7927268PMC
March 2021

Encapsulating VO Nanoparticles in Hierarchical Porous Carbon Nanosheets via C-O-V Bonds for Fast and Durable Potassium-Ion Storage.

ACS Appl Mater Interfaces 2021 Mar 3;13(10):12149-12158. Epub 2021 Mar 3.

School of Metallurgy and Environment, Central South University, Changsha 410083, China.

Vanadium oxide (VO) has been considered as a promising anode material for potassium-ion batteries (PIBs), but challenging as well for the low electron/ion conductivity and poor structural stability. To tackle these issues, herein, a novel sheetlike hybrid nanoarchitecture constructed by uniformly encapsulating VO nanoparticles in amorphous carbon nanosheets ([email protected]) with the generation of C-O-V bonding is presented. Such a subtle architecture effectively facilitates the infiltration of electrolyte, relieves the mechanical strain, and reduces the potassium-ion diffusion distance during the repetitive charging/discharging processes. The generated C-O-V bonding not only accelerated charge transfer across the carbon-VO interface but also strengthened the structural stability. Benefiting from the synergistic effects, the as-prepared [email protected] nanosheets display fast and durable potassium storage behaviors with a reversible capacity of 116.6 mAh g delivered at 5 A g, and a specific capacity of 147.9 mAh g retained after 1800 cycles at a high current density of 2 A g. Moreover, the insertion/extraction mechanism of [email protected] nanosheets in potassium-ion storage is systematically demonstrated by electrochemical analysis and ex situ technologies. This study will shed light on the fabricating of other metal oxides anodes for high-performance PIBs and beyond.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acsami.1c01303DOI Listing
March 2021

Epothilone B prevents lipopolysaccharide-induced inflammatory osteolysis through suppressing osteoclastogenesis via STAT3 signaling pathway.

Aging (Albany NY) 2020 06 11;12(12):11698-11716. Epub 2020 Jun 11.

Department of Biomedical Materials Science, Third Military Medical University (Army Medical University), Chongqing 400038, China.

Inflammatory osteolysis is a common osteolytic specificity that occurs during infectious orthopaedic surgery and is characterized by an imbalance in bone homeostasis due to excessive osteoclast bone resorption activity. Epothilone B (Epo B) induced α-tubulin polymerization and enhanced microtubule stability, which also played an essential role in anti-inflammatory effect on the regulation of many diseases. However, its effects on skeletal system have rarely been investigated. Our study demonstrated that Epo B inhibited osteoclastogenesis and prevented inflammatory osteolysis Further analysis showed that Epo B also markedly induced mature osteoclasts apoptosis during osteoclastogenesis. Mechanistically, Epo B directly suppressed osteoclastogenesis by the inhibitory regulation of the phosphorylation and activation of PI3K/Akt/STAT3 signaling directly, and the suppressive regulation of the CD9/gp130/STAT3 signaling pathway indirectly. The negative regulatory effect on STAT3 signaling further restrained the translocation of NF-κB p65 and NFATc1 from the cytosol to the nuclei during RANKL stimulation. Additionally, the expression of osteoclast specific genes was also significantly attenuated during osteoclast fusion and differentiation. Taken together, these findings illustrated that Epo B protected against LPS-induced bone destruction through inhibiting osteoclastogenesis via regulating the STAT3 dependent signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/aging.103337DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343516PMC
June 2020

Dual-Peptide-Functionalized Nanofibrous Scaffolds Recruit Host Endothelial Progenitor Cells for Vasculogenesis to Repair Calvarial Defects.

ACS Appl Mater Interfaces 2020 Jan 10;12(3):3474-3493. Epub 2020 Jan 10.

Orthopedic Department, Southwest Hospital , The First Hospital Affiliated to Army Medical University (Southwest Hospital) , Chongqing 400038 , P.R. China.

Vasculogenesis (de novo formation of vessels) induced by endothelial progenitor cells (EPCs) is requisite for vascularized bone regeneration. However, there exist few available options for promoting vasculogenesis within artificial bone grafts except for exogenous EPC transplantation, which suffers from the source of EPC, safety, cost, and time concerns in clinical applications. This study aimed at endogenous EPC recruitment for vascularized bone regeneration by using a bioinspired EPC-induced graft. The EPC-induced graft was created by immobilizing two bioactive peptides, WKYMVm and YIGSR, on the surface of poly(ε-caprolactone) (PCL)/poliglecaprone (PGC) nanofibrous scaffolds via a polyglycolic acid (PGA)-binding peptide sequence. Remarkable immobilization efficacy of WKYMVm and YIGSR peptides and their sustained release (over 14 days) from scaffolds were observed. In vivo and in vitro studies showed robust recruitment of EPCs, which subsequently contributed to early vasculogenesis and ultimate bone regeneration. The dual-peptide-functionalized nanofibrous scaffolds proposed in this study provide a promising therapeutic strategy for vasculogenesis in bone defect repair.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acsami.9b21434DOI Listing
January 2020

Engineering Hollow Porous Carbon-Sphere-Confined MoS with Expanded (002) Planes for Boosting Potassium-Ion Storage.

ACS Appl Mater Interfaces 2020 Jan 20;12(1):1232-1240. Epub 2019 Dec 20.

School of Metallurgy and Environment , Central South University , Changsha 410083 , China.

Potassium-ion batteries (PIBs) are emerging as promising next-generation electrochemical storage systems for their abundant and low-cost potassium resource. The key point of applying PIBs is to exploit stable K-host materials to accommodate the large-sized potassium ion. In this work, a yolk-shell structured [email protected] porous carbon-sphere composite ([email protected]) assembled by engineering HPCS-confined MoS with expanded (002) planes is proposed for boosting potassium-ion storage. When used as a PIB anode, the as-synthesized [email protected] composite shows superior potassium storage performance. It delivers a reversible capacity of 254.9 mAh g at 0.5 A g after 100 discharge/charge cycles and maintains 126.2 mAh g at 1 A g over 500 cycles. The superior potassium-ion storage performance is ascribed to the elaborate yolk-shell nanoarchitecture and the expanded interlayer of the MoS nanosheet, which could shorten the transport distance, enhance the electronic conductivity, relieve the volume variation, prevent the self-aggregation of MoS, facilitate the electrolyte penetration, and boost the intercalation/deintercalation of K. Moreover, the potential application of the [email protected] composite is also evaluated by assembled K-ion full cells with a perylenetetracarboxylic dianhydride cathode. Accordingly, the as-developed synthetic strategy can be extended to manufacture other host materials for PIBs and beyond.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acsami.9b14742DOI Listing
January 2020

The protective effect of WKYMVm peptide on inflammatory osteolysis through regulating NF-κB and CD9/gp130/STAT3 signalling pathway.

J Cell Mol Med 2020 01 14;24(2):1893-1905. Epub 2019 Dec 14.

Department of Orthopedics, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.

The balance between bone formation and bone resorption is closely related to bone homeostasis. Osteoclasts, originating from the monocyte/macrophage lineage, are the only cell type possessing bone resorption ability. Osteoclast overactivity is thought to be the major reason underlying osteoclast-related osteolytic problems, such as Paget's disease, aseptic loosening of prostheses and inflammatory osteolysis; therefore, disruption of osteoclastogenesis is considered a crucial treatment option for these issues. WKYMVm, a synthetic peptide, which is a potent FPR2 agonist, exerts an immunoregulatory effect. This peptide inhibits the production of inflammatory cytokines, such as (IL)-1β and TNF-α, thus regulating inflammation. However, there are only few reports on the role of WKYMVm and FPR2 in osteoclast cytology. In the current study, we found that WKYMVm negatively regulates RANKL- and lipopolysaccharide (LPS)-induced osteoclast differentiation and maturation in vitro and alleviates LPS-induced osteolysis in animal models. WKYMVm down-regulated the expression of osteoclast marker genes and resorption activity. Furthermore, WKYMVm inhibited osteoclastogenesis directly through reducing the phosphorylation of STAT3 and NF-kB and indirectly through the CD9/gp130/STAT3 pathway. In conclusion, our findings demonstrated the potential medicinal value of WKYMVm for the treatment of inflammatory osteolysis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/jcmm.14885DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6991638PMC
January 2020

Interleukin-27 prevents LPS-induced inflammatory osteolysis by inhibiting osteoclast formation and function.

Am J Transl Res 2019 15;11(3):1154-1169. Epub 2019 Mar 15.

Department of Orthopedics, Guizhou Province People's Hospital Guiyang 550002, China.

Osteolysis is a serious complication of several chronic inflammatory diseases and is closely associated with a local chronic inflammatory reaction with a variety of causes. Inflammatory factors and osteoclastogenesis can enhance bone erosion. Interleukin-27 (IL-27) is speculated to play an important role in the physiological immune response. However, there are few studies on its effects on osteoclastogenesis. In this study, IL-27 was shown to inhibit receptor activator nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. The gene expression levels of osteoclast (OC)-specific genes, such as nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and C-FOS, which are essential for OC differentiation and bone resorption, were significantly reduced. Further investigating the underlying mechanism, we found that IL-27 significantly reduced RANKL-induced osteoclastogenesis by inhibiting the phosphorylation of IκB and phosphorylation of nuclear factor κB (NF-κB) p65. Furthermore, IL-27 was shown to inhibit lipopolysaccharide (LPS)-induced osteolysis in vivo. Collectively, these results indicate that IL-27 may be a potential candidate for the treatment of osteolytic diseases.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456512PMC
March 2019
-->