Ionic liquids intercalation in titanium carbide MXenes: A first-principles investigation.

Herein, we present a density functional theory with dispersion correction (DFT-D) calculations that focus on the intercalation of ionic liquids (ILs) electrolytes into the two-dimensional (2D) Ti3C2Tx MXenes. These ILs include the cation 1-ethyl-3-methylimidazolium (Emim+), accompanied by three distinct anions: bis(trifluoromethylsulfonyl)imide (TFSA-), (fluorosulfonyl)imide (FSA-) and fluorosulfonyl(trifluoromethanesulfonyl)imide (FTFSA-). By altering the surface termination elements, we explore the intricate geometries of IL intercalation in neutral, negative, and positive pore systems. Accurate estimation of charge transfer is achieved through five population analysis models, such as Hirshfeld, Hirshfeld-I, DDEC6 (density derived electrostatic and chemical), Bader, and VDD (voronoi deformation density) charges. In this work, we recommend the DDEC6 and Hirshfeld-I charge models, as they offer moderate values and exhibit reasonable trends. The investigation, aimed at visualizing non-covalent interactions, elucidates the role of cation-MXene and anion-MXene interactions in governing the intercalation phenomenon of ionic liquids within MXenes. The magnitude of this role depends on two factors: the specific arrangement of the cation, and the nature of the anionic species involved in the process.

Interrupted time series analysis using the ARIMA model of the impact of COVID-19 on the incidence rate of notifiable communicable diseases in China.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic in China is ongoing. Some studies have shown that the incidence of respiratory and intestinal infectious diseases in 2020 decreased significantly compared with previous years. Interrupted time series (ITS) is a time series analysis method that evaluates the impact of intervention measures on outcomes and can control the original regression trend of outcomes before and after the intervention. This study aimed to analyse the impact of COVID-19 on the incidence rate of notifiable communicable diseases using ITS in China. METHODS: National data on the incidence rate of communicable diseases in 2009-2021 were obtained from the National Health Commission website. Interrupted time series analysis using autoregressive integrated moving average (ARIMA) models was used to analyse the changes in the incidence rate of infectious diseases before and after the COVID-19 epidemic. RESULTS: There was a significant short-term decline in the incidence rates of respiratory infectious diseases and enteric infectious diseases (step values of -29.828 and - 8.237, respectively), which remained at a low level for a long time after the decline. There was a short-term decline in the incidence rates of blood-borne and sexually transmitted infectious diseases (step = -3.638), which tended to recover to previous levels in the long term (ramp = 0.172). There was no significant change in the incidence rate of natural focus diseases or arboviral diseases before and after the epidemic. CONCLUSION: The COVID-19 epidemic had strong short-term and long-term effects on respiratory and intestinal infectious diseases and short-term control effects on blood-borne and sexually transmitted infectious diseases. Our methods for the prevention and control of COVID-19 can be used for the prevention and control of other notifiable communicable diseases, especially respiratory and intestinal infectious diseases.

Hexapeptide induces M2 macrophage polarization via the JAK1/STAT6 pathway to promote angiogenesis in bone repair.

Angiogenesis is essential for successful bone defect repair. In normal tissue repair, the physiological inflammatory response is the main regulator of angiogenesis through the activity of macrophages and the cytokines secreted by them. In particular, M2 macrophages which secrete high levels of PDGF-BB are typically considered to promote angiogenesis. A hexapeptide [WKYMVm, (Trp-Lys-Tyr-Met-Val-D-Met-NH2)] has been reported to modulate inflammatory activities. However, the underlying mechanisms by which WKYMVm regulates macrophages remain unclear. In this study, the possible involvement by which WKYMVm induces the polarization of macrophages and affects their behaviors was evaluated. In vitro results showed that macrophages were induced to an M2 rather than M1 phenotype and the M2 phenotype was enhanced by WKYMVm through activation of the JAK1/STAT6 signaling pathway. It was also found that WKYMVm played an important role in the PDGF-BB production increase and proangiogenic abilities in M2 macrophages. Consistent with the results in vitro, the elevated M2/M0 ratio induced by WKYMVm enhanced the formation of new blood vessels in a femoral defect mouse model. These findings suggest that WKYMVm could be a promising alternative strategy for angiogenesis in bone repair by inducing M2 macrophage polarization.

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

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 CD31highEmcnhigh 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 (Pr3+, Nd3+, Sm3+). 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.

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

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)-1ß 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.

Preparation and drug release performance of different gelation type polysaccharide/ß-lactoglobulin fiber composite gels.

Self-assembled protein fibers have attracted much attention in the fields of medicine and food because of their high aspect ratio, polymorphic structure and strong surface hydrophobicity. In this study, three different gelation types of polysaccharides/ß-lactoglobulin fiber (Fblg) composite gels, including ionic alginate-Fblg gels, synergistic xanthan-Fblg gels, and double network agar-Fblg gels, were first prepared. The interactions between the polysaccharides and the Fblgs, the microstructure and mechanical properties of the composite gels were investigated using the light scattering, scanning electron microscopy, rheology and texture analysis in order to reveal their formation mechanisms. Then the loading and release properties of the water-soluble drug 5-fluorouracil (5-FU) and the hydrophobic drug curcumin (Cur) through these composite gels were further studied with release mechanisms determined by fitting different release models. It was found that the mechanical properties of the composite gels were determined by the mesh density of the three-dimensional networks formed inside the gels. The network structure and mechanical strength of the alginate-Fblg gels became weaker with the increase of Fblg content at pH 4 due to their attractive interaction which hindered the binding of Ca2+ to ALG, while the network and the strength of the alginate-Fblg gels didn't change much at pH 7 due to the repulsion between Alg and Fblg. The xanthan-Fblg gels formed lamellar structures with enhanced gel network and mechanical strength due to the hydrogen bonding and the electrostatic interaction with Fblg. The Agar-Fblg composite gel formed at 60 °C (above the gelation temperature of agar of 40 °C) had a denser double network structure and higher mechanical strength than that formed at 0 °C due to inhibition of diffusion of Ca2+ as salt bridges for Fblg. The hydrophilic drugs were loaded in the meshes of the composite gels and their release was determined by the structure of the composite gel networks, whereas the hydrophobic drugs were loaded by attaching to the Fblgs in the composite gels and their release was determined by the loading ability and strength of the gels. The study not only provided a new idea for the preparation and application of polysaccharide-protein fiber composite hydrogels, but also provided insights for improving the efficiency of drug carriers.

Rab26 promotes macrophage phagocytosis through regulation of MFN2 trafficking to mitochondria.

Acute respiratory distress syndrome (ARDS) is an inflammatory disorder of the lungs caused by bacterial or viral infection. Timely phagocytosis and clearance of pathogens by macrophages are important in controlling inflammation and alleviating ARDS. However, the precise mechanism of macrophage phagocytosis remains to be explored. Here, we show that the expression of Rab26 is increased in Escherichia coli- or Pseudomonas aeruginosa-stimulated bone marrow-derived macrophages. Knocking out Rab26 reduced phagocytosis and bacterial clearance by macrophages. Rab26 interacts with mitochondrial fusion protein mitofusin-2 (MFN2) and affects mitochondrial reactive oxygen species generation by regulating MFN2 transport. The levels of MFN2 in mitochondria were reduced in Rab26-deficient bone marrow-derived macrophages, and the levels of mitochondrial reactive oxygen species and ATP were significantly decreased. Knocking down MFN2 using small interfering RNA resulted in decreased phagocytosis and killing ability of macrophages. Rab26 knockout reduced phagocytosis and bacterial clearance by macrophages in vivo, significantly increased inflammatory factors, aggravated lung tissue damage, and increased mortality in mice. Our results demonstrate that Rab26 regulates phagocytosis and clearance of bacteria by mediating the transport of MFN2 to mitochondria in macrophages, thus alleviating ARDS in mice and potentially in humans.

Boosting potassium-storage performance via confining highly dispersed molybdenum dioxide nanoparticles within N-doped porous carbon nano-octahedrons.

The development of durable and stable metal oxide anodes for potassium ion batteries (PIBs) has been hampered by poor electrochemical performance and ambiguous reaction mechanisms. Herein, we design and fabricate molybdenum dioxide (MoO2)@N-doped porous carbon (NPC) nano-octahedrons through metal-organic frameworks derived strategy for PIBs with MoO2 nanoparticles confined within NPC nano-octahedrons. Benefiting from the synergistic effect of nanoparticle level of MoO2 and N-doped carbon porous nano-octahedrons, the MoO2@NPC electrode exhibits superior electron/ion transport kinetics, excellent structural integrity, and impressive potassium-ion storage performance with enhanced cyclic stability and high-rate capability. The density functional theory calculations and experiment test proved that MoO2@NPC has a higher affinity of potassium and higher conductivity than MoO2 and N-doped carbon electrodes. Kinetics analysis revealed that surface pseudocapacitive contributions are greatly enhanced for MoO2@NPC nano-octahedrons. In-situ and ex-situ analysis confirmed an intercalation reaction mechanism of MoO2@NPC for potassium ion storage. Furthermore, the assembled MoO2@NPC//perylenetetracarboxylic dianhydride (PTCDA) full cell exhibits good cycling stability with 72.6 mAh g-1 retained at 100 mA g-1 over 200 cycles. Therefore, this work present here not only evidences an effective and viable structural engineering strategy for enhancing the electrochemical behavior of MoO2 material in PIBs, but also gives a comprehensive insight of kinetic and mechanism for potassium ion interaction with metal oxide.

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

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.

An advanced BiPO4/super P anode material for high-performance potassium-ion batteries.

Dispersed BiPO4 nanoparticles loaded on the surface of a super P conducting network (BiPO4/SP) were fabricated and investigated as a novel anode for PIBs. The BiPO4/SP electrode demonstrates high rate capability (97.1 mA h g-1 at 500 mA g-1) and good long-term cycling performance (116 mA h g-1 at 200 mA g-1 over 100 cycles).

Encapsulating V2O3 Nanoparticles in Hierarchical Porous Carbon Nanosheets via C-O-V Bonds for Fast and Durable Potassium-Ion Storage.

Vanadium oxide (V2O3) 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 V2O3 nanoparticles in amorphous carbon nanosheets (V2O3@C) 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-V2O3 interface but also strengthened the structural stability. Benefiting from the synergistic effects, the as-prepared V2O3@C nanosheets display fast and durable potassium storage behaviors with a reversible capacity of 116.6 mAh g-1 delivered at 5 A g-1, and a specific capacity of 147.9 mAh g-1 retained after 1800 cycles at a high current density of 2 A g-1. Moreover, the insertion/extraction mechanism of V2O3@C 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.

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

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.

Insights into the simultaneous nitrification, denitrification and phosphorus removal process for in situ sludge reduction and potential phosphorus recovery.

A simultaneous nitrification-denitrification and phosphorus removal (SNDPR) system operated in an alternating anaerobic/aerobic/anoxic (A/O/A) mode was revisited from new perspectives of sludge reduction and potential phosphorus recovery. Reliable and robust removal performance was obtained even under winter temperatures, with average removal efficiency of COD, TP, NH4+-N and TIN being 89.68%, 93.60%, 92.15% and 79.01% at steady state, respectively. Inoculated sludge got enhanced in biomass density, settleability, and bioactivity. And relatively stable amounts of extracellular polymeric substances (EPS) with a stable protein/ polysaccharide (PN/PS) ratio were observed over operation. Meanwhile, a low observed sludge yield (Yobs) of 0.083 g MLSS/g COD (0.082 g MLVSS/g COD) was obtained. A maximum anaerobic phosphorus release up to 43.54 mg/L was found, thus providing phosphorus-rich and low-turbidity stream for further phosphorus recovery. Overall, the SNDPR system deserved attention for in situ sludge reduction and potential phosphorus recovery, beyond reliable and stable wastewater treatment.

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

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-1ß, IL-6, IL-12 and TNF-α inflammatory factors were measured using kits. The expression of GSK-3ß, 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-3ß/NF-κB/CREB pathway, suggesting that FA can be used to protect the liver against ALI.

Engineering Hollow Porous Carbon-Sphere-Confined MoS2 with Expanded (002) Planes for Boosting Potassium-Ion Storage.

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 MoS2@hollow porous carbon-sphere composite (MoS2@HPCS) assembled by engineering HPCS-confined MoS2 with expanded (002) planes is proposed for boosting potassium-ion storage. When used as a PIB anode, the as-synthesized MoS2@HPCS composite shows superior potassium storage performance. It delivers a reversible capacity of 254.9 mAh g-1 at 0.5 A g-1 after 100 discharge/charge cycles and maintains 126.2 mAh g-1 at 1 A g-1 over 500 cycles. The superior potassium-ion storage performance is ascribed to the elaborate yolk-shell nanoarchitecture and the expanded interlayer of the MoS2 nanosheet, which could shorten the transport distance, enhance the electronic conductivity, relieve the volume variation, prevent the self-aggregation of MoS2, facilitate the electrolyte penetration, and boost the intercalation/deintercalation of K+. Moreover, the potential application of the MoS2@HPCS 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.

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

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 in vitro and prevented inflammatory osteolysis in vivo. 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.

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

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.

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

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.