Study of Modified Offset Trajectory for Bonnet Polishing Based on Lifting Bonnet Method.

The inability to converge at the edge of a workpiece during polishing affects the edge profile accuracy and surface quality of the workpiece. In this study, a bias trajectory generation method based on the lifting bonnet method that can maintain the morphology of polished edges is presented. Firstly, by establishing the polishing parameters and the decreasing rule in line with the principles of the lifting bonnet method, we obtained the residual height spacing, the radius of the polishing area, the centre offset position, and the pressing depth for each offset trajectory. Subsequently, the modified bias trajectory algorithm correction coefficients were obtained by fitting the edge trajectories using cubic Bessel curves, which were multiplied with the bias amount to obtain the final modified bias trajectory. Finally, an experiment was designed to compare the edge effect of the modified bias trajectory with the traditional grating trajectory. The experimental findings indicate that the reduction in edge collapse following the implementation of the modified offset trajectory was 1.30 µm. In contrast, the edge collapse after polishing with the traditional grating trajectory amounted to 98.67 µm. Moreover, the edge collapse ensuing traditional polishing trajectory was 75.9 times more pronounced than that observed after using the modified offset trajectory. It is shown that the modified bias trajectory method can not only maintain the original edge morphology of the workpiece but can also promote the convergence of the edge effect to a certain extent.

Effects of astragaloside IV on glucocorticoid-induced avascular necrosis of the femoral head via regulating Akt-related pathways.

We investigated the role of astragaloside IV (AS-IV) in preventing glucocorticoid-induced avascular necrosis of the femoral head (ANFH) and the underlying molecular mechanisms. Network pharmacology was used to predict the molecular targets of AS-IV. Molecular dynamic simulations were performed to explore the binding mechanism and interaction mode between AS-IV and Akt. Rat models of glucocorticoid-induced ANFH with AS-IV intervention were established, and osteogenesis, angiogenesis, apoptosis and oxidative stress were evaluated before and after blocking the PI3K/Akt pathway with LY294002. The effects of glucocorticoid and AS-IV on bone marrow mesenchymal stem cells and human umbilical vein endothelial cells incubated with and without LY294002 were determined. Downregulated p-Akt expression could be detected in the femoral heads of glucocorticoid-induced ANFH patients and rats. AS-IV increased trabecular bone integrity and vessel density of the femoral head in the model rats. AS-IV increased Akt phosphorylation and upregulated osteogenesis-, angiogenesis-, apoptosis- and oxidative stress-related proteins and mRNA and downregulated Bax, cleaved caspase-3 and cytochrome c levels. AS-IV promoted human umbilical vein endothelial cell migration, proliferation and tube formation ability; bone marrow mesenchymal stem cell proliferation; and osteogenic differentiation under glucocorticoid influence. AS-IV inhibited apoptosis. LY294002 inhibited these effects. AS-IV prevented glucocorticoid-induced ANFH by promoting osteogenesis and angiogenesis via the Akt/Runx2 and Akt/HIF-1α/VEGF pathways, respectively, and suppressing apoptosis and oxidative stress via the Akt/Bad/Bcl-2 and Akt/Nrf2/HO-1 pathways, respectively.

Cornuside ameliorates cognitive impairments in scopolamine induced AD mice: Involvement of neurotransmitter and oxidative stress.

ETHNOPHARMACOLOGICAL RELEVANCE: Cornus officinalis Sieb. et Zucc., traditional Chinese medicine, has been widely used in the treatment of dementia. Cornel iridoid glycosides of Cornus officinalis is therapeutic to Alzheimer's disease (AD), while its pharmacodynamic material basis is not clear. Cornuside, an iridoid glycoside extracted from of Cornus officinalis Sieb. et Zucc, might be a potential anti-AD candidate. AIM OF THE STUDY: Cornuside was evaluated for its effect on scopolamine induced AD mice, and its action mechanisms were explored. MATERIALS AND METHODS: ICR mice were administered with 1 mg/kg scopolamine intraperitoneally to induce amnesia. The therapeutic effect of cornuside of cognitive function was evaluated via series of behavioral tests, including Morris water maze test, step-through test and step-down test. In addition, specific enzyme reaction tests were used to detect the content of acetylcholine (ACh) and malondialdehyde (MDA), as well as the activities of acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), choline acetyltransferase (ChAT), superoxide dismutase (SOD), catalase (CAT), monoamine oxidase (MAO) in the brain. The levels of monoamine neurotransmitters were detected by high performance liquid chromatography-electrochemical detection (HPLC-ECD). RESULTS: Cornuside ameliorated the spatial memory impairment in Morris water maze test and cognitive disruption in step-through and step-down test. Furthermore, cornuside improved the level of ACh by reducing the activities of AChE and BuChE, and increasing the activity of ChAT in hippocampus. Cornuside also increased the levels of monoamine neurotransmitters by inhibiting MAO activity in hippocampus and cortex. In addition, cornuside attenuated MDA by enhancing the activities of SOD and CAT in hippocampus and cortex. CONCLUSION: Cornuside improved cognitive dysfunction induced by scopolamine in behavioral tests. The mechanisms of cornuside were further investigated from the aspects of neurotransmitters and oxidative stress. Cornuside could inhibit oxidative stress and neurotransmitter hydrolases, increase ACh and monoamine neurotransmitters, which finally contributed to its therapeutic effect on scopolamine induced amnesia.

miR-146a Protects against Staphylococcus aureus-Induced Osteomyelitis by Regulating Inflammation and Osteogenesis.

Osteomyelitis is a Staphylococcus aureus-caused bone infection. In this study, the effects of miR-146a on osteomyelitis were evaluated. Using the osteoblast cell model and S. aureus-induced osteomyelitis mice model, we monitored the miR-146 expression and explored the effects of miR-146a on cell proliferation of osteoblasts, bone remodeling, osteoclastogenesis, inflammatory cytokine production, and bacterial burden. Upregulated miR-146a was found in mice with S. aureus-induced osteomyelitis. miR-146a attenuated S. aureus-induced cell loss of osteoblasts, rescued the expression of osteogenic markers, altered the bone remodeling, and inhibited inflammatory cytokine production and osteoclastogenesis. miR-146a knockout mice had higher S. aureus burden. In conclusion, miR-146a protects against S. aureus-induced osteomyelitis by regulating inflammation and osteogenesis.

Binder-free Fe-doped NiCo2O4/Ni3S4 hollow heterostructure nanotubes for highly efficient overall water splitting.

For overall water splitting, a vital challenge is to design active sites at interfaces. Heterogeneous catalysts with enhanced mass/charge transfer and accelerated adsorption of intermediates have exhibited significantly enhanced activities. Herein, a Fe-doped NiCo2O4/Ni3S4 heterogeneous electrocatalyst is synthesized for the HER and OER. On account of the synergistic effect of heterostructures, Ni-O-S presents a low overpotential of 29.1 mV (10 mA cm-2), a relatively small Tafel slope of 53.3 mV dec-1 for the HER, and 259 mV at a current density of 100 mA cm-2 (33.1 mV dec-1) for the OER. What is more, Ni-O-S acts as a binder-free bi-functional electrode in an alkaline electrolyte for overall water splitting, exhibiting a cell voltage of 1.45 V (10 mA cm-2) with good stability. This work offers an efficient approach for designing stable and high-efficiency heterogeneous electrodes for overall water splitting.

Loganin ameliorates depression-like behaviors of mice via modulation of serotoninergic system.

RATIONALE: Depression is a serious neuropsychiatric disorder, which is characterized by sustaining mood disorders. Loganin, a major iridoid glycoside from Corni fructus, has a variety of pharmacological activities, including neuroprotective effect and hypnotic effect. However, little is known about the effects of loganin on stress-induced depression. OBJECTIVE: To investigate the effects of loganin on behavioral despair of mice, and whether serotonin (5-HT) and/or noradrenaline (NE) are involved in this process. METHODS: We tested the effectiveness of loganin using tail suspension test (TST). The possible mechanism was explored using reserpine-induced ptosis and hypothermia, and 5-HTP-induced head-twitch response in mice. The changes of 5-HT and NE in the prefrontal cortex, hippocampus, and striatum were measured through high-performance liquid chromatography (HPLC) analysis. Then, we identified the effects of depleting 5-HT and NE by PCPA (p-chlorophenylalanine) and DSP-4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride) pretreatment, respectively. RESULTS: Loganin (12.5/50 mg/kg) induced antidepressant-like effects in mice submitted to TST. Loganin (12.5/50 mg/kg) ameliorated the reserpine-induced hypothermia and ptosis, as well as increased 5-HTP-induced head-twitch responses in mice. Loganin (50 mg/kg) significantly increased the levels of 5-HT in the prefrontal cortex, hippocampus, and striatum. Furthermore, only PCPA treatment could eliminate loganin-induced antidepressant-like effects in TST. CONCLUSION: Loganin exerts antidepressant-like effect in the TST depending on 5-HT levels in the central nervous system, which provide a potential agent for depression therapy.

Antineoplastic Effects and Mechanisms of a New RGD Chimeric Peptide from Bullfrog Skin on the Proliferation and Apoptosis of B16F10 Cells.

Malignant melanoma, an increasingly common form of skin cancer, poses a significant threat to public health, especially when the disease progresses past skin lesions to the stage of advanced metastasis. In this work, a new anti-tumor peptide, temporin La (T-La), was selected from a cDNA library generated from bullfrog skin. Two new derivative antitumor peptides, T-La (S) and T-La (FS), were designed by bioinformatics analysis and coupled with the RGD small molecule peptide to create chimeric RGD peptides, (RGD-T-La [S] and RGD-T-La [FS]). Preliminary experiments showed that the new antitumor peptides had significant antitumor effects. After coupling to the chimeric RGD peptide, the targeted treatment of mouse melanoma was significantly improved. Our data demonstrate that the 4 peptides tested herein significantly inhibited the proliferation, migration, and invasion of B16F10 cells; with an increase in polypeptide concentration, the proportion of melanoma cells in the G0/G1 phase decreased or increased significantly, respectively, the reactive oxygen species (ROS) content increased significantly, the mitochondrial membrane potential decreased significantly, and the expression of pro-apoptotic Bax, Caspase-3, and Caspase-9 increased, and anti-apoptotic Bcl-2 decreased significantly. Tyr and MITF genes were significantly downregulated. In conclusion, the use of these new anti-tumor peptides, when combined with a chimeric RGD peptide, may increase ROS levels and decrease mitochondrial membrane potential by inhibiting the activity of mitochondria, thus releasing apoptosis-promoting factors in B16F10 cells. The present study describes a new potential strategy for the application of promising peptides in the treatment of various cancers.

IL-15 deficiency alleviates steroid-induced osteonecrosis of the femoral head by impact osteoclasts via RANKL-RANK-OPG system.

BACKGROUND: Whether IL-15 is involved in the development of steroid-induced osteonecrosis of the femoral head (ONFH) is investigated. METHODS: C57BL/6 J and l15-/-mice were injected with methylprednisolone to induce wide type osteonecrosis (WT ON) and IL-15 deficiency osteonecrosis (IL-15-/- ON). Hematoxylin-Eosin (H&E) staining and micro-computed tomography (micro-CT) scanning was used to detect the microstructure. The differentiation and formation of osteoclasts were determined with colony-forming unit-granulocyte macrophages (CFU-GM), colony-forming unit-macrophage/mononuclear (CFU-M) per tibia, and tartrate-resistant acid phosphatase (TRACP or TRAP) positive cells. Serum interleukin (IL)-15, osteocalcin, bone alkaline phosphatase (BAP), bone Gla protein (BGP), and TRACP were assayed with enzyme-linked immunosorbent assay (ELISA). The receptor activator of nuclear factor-κB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) in the femoral heads were detected by Western blot. CD34 staining was performed to detect microvascular density. RESULTS: IL-15 secretion was increased in the femoral heads and the serum of steroid-induced ONFH mice. IL-15 deficiency may lead to up-regulated vessel remodeling, improved microstructure, and up-regulated serum osteocalcin, BAP, and BGP secretion. Both the expression of RANKL/RANK/OPG and osteoclast differentiation and formation can be down-regulated by IL-15 deficiency. CONCLUSION: IL-15 deficiency alleviates steroid-induced ONFH by impact osteoclasts via RANKL-RANK-OPG system.

Connexins in oligodendrocytes and astrocytes: Possible factors for demyelination in multiple sclerosis.

Increasing evidences support that glial connexins are involved in the demyelination pathology of multiple sclerosis (MS), a chronic inflammatory demyelinating disorder. Here, we review the data from patients with MS and animal models of MS that implicate connexins in demyelination. Connexins expressed in oligodendrocytes and astrocytes show diverse changes at the different phases of MS. Loss of oligodendrocyte or astrocyte connexins contributes to demyelination and exaggerates the pathology of MS. Channel-dependent and -independent connexins are involved in the pathology of demyelination, which is related with myelin integrity, metabolic homeostasis, the brain-blood barrier, the immune cell infiltration, and the inflammatory response. A comprehensive understanding of connexin function in demyelination may provide new therapeutic targets for MS.

The promotion of bone regeneration through CS/GP-CTH/antagomir-133a/b sustained release system.

Few studies reported the application of miRNA in bone regeneration. In this study, the expression of miR133a and miR133b in murine BMSCs was inhibited via antagomiR-133a/b and the osteogenic differentiation in murine BMSCs was evaluated. The RT-PCR, flow cytometry, cell counting kit-8, and annexin V-FITC/PI double staining assays were performed. Double knockdown miR133a and miR133b can promote BMSC osteogenic differentiation. At optimum N/P ration (15:1), the loading efficiency can reach over 90%. CTH-antagomiR-133a/b showed no cytotoxicity to BMSCs and diminished miR133a and miR133b expression in BMSCs. Furthermore, chitosan-based sustained delivery system can facilitate continuous dosing of antagomiR-133a/b, which enhanced calcium deposition and osteogenic specific gene expression in vitro. The new bone formation was enhanced after the sustained delivery system containing CTH-antagomiR-133a/b nanoparticles was used in mouse calvarial bone defect model. Our results demonstrate that CTH nanoparticles could facilitate continuous dosing of antagomiR133a/b, which can promote osteogenic differentiation.

Inhibition of microRNA-222 up-regulates TIMP3 to promotes osteogenic differentiation of MSCs from fracture rats with type 2 diabetes mellitus.

Type 2 diabetes mellitus (T2DM) is the most common diabetes and has numerous complications. Recent studies demonstrated that T2DM compromises bone fracture healing in which miR-222 might be involved. Furthermore, tissue inhibitor of metalloproteinase 3 (TIMP-3) that is the target of miR-222 accelerates fracture healing. Therefore, we assume that miR-222 could inhibit TIMP-3 expression. Eight-week-old rats were operated femoral fracture or sham, following the injection of streptozotocin (STZ) to induce diabetes one week later in fractured rats, and then, new generated tissues were collected for measuring the expression of miR-222 and TIMP-3. Rat mesenchymal stem cells (MSCs) were isolated and treated with miR-222 mimic or inhibitor to analyse osteogenic differentiation. MiR-222 was increased in fractured rats and further induced in diabetic rats. In contrast, TIMP-3 was reduced in fractured and further down-regulated in diabetic rats. Luciferase report assay indicated miR-222 directly binds and mediated TIMP-3. Furthermore, osteogenic differentiation was suppressed by miR-222 mimic and promoted by miR-222 inhibitor. miR-222 is a key regulator that is promoted in STZ-induced diabetic rats, and it binds to TIMP3 to reduce TIMP-3 expression and suppressed MSCs' differentiation.

ATP6V1H facilitates osteogenic differentiation in MC3T3-E1 cells via Akt/GSK3ß signaling pathway.

Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of all diabetic patients, and osteoporosis is one of the complications during T2DM process. ATP6V1H (V-type proton ATPase subunit H) displays crucial roles in inhibiting bone loss, but its role in osteogenic differentiation remains unknown. Therefore in this study, we aimed to explore the biological role of ATP6V1H in osteogenic differentiation. OM (osteogenic medium) and HG (high glucose and free fatty acids) were used to induce the MC3T3-E1 cells into osteogenic differentiation in a T2DM simulating environment. CCK8 assay was used to detect cell viability. Alizarin Red staining was used to detect the influence of ATP6V1H on osteogenic differentiation. ATP6V1H expression increased in OM-MC3T3-E1 cells, while decreased in OM+HG-MC3T3-E1 cells. ATP6V1H promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. Overexpression of ATP6V1H inhibited Akt/GSK3ß signaling pathway, while knockdown of ATP6V1H promoted Akt/GSK3ß signaling pathway. ATP6V1H overexpression promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. The role of ATP6V1H in osteogenic differentiation in a T2DM simulating environment involved in Akt/GSK3ß signaling pathway. These data demonstrated that ATP6V1H could serve as a potential target for osteogenic differentiation in a T2DM simulating environment.

6-Bromoindirubin-3'-Oxime (6BIO) Suppresses the mTOR Pathway, Promotes Autophagy, and Exerts Anti-aging Effects in Rodent Liver.

Liver aging is associated with age-related histopathological and functional changes that significantly enhance the risk of numerous diseases or disorders developing in elderly populations. 6-Bromoindirubin-3'-oxime (6BIO), a potent inhibitor of glycogen synthase kinase-3 (GSK-3), has been implicated in various age-related diseases and processes, such as tumorigenesis, neurodegeneration, and diabetes. Recent studies have also revealed that 6BIO increases autophagy in yeast, mammalian cell lines, and dopaminergic neurons, which is one of the classical mechanisms strongly associated with liver aging. However, the impact or the mechanism of action of 6BIO in liver remains entirely unknown. Here, we find that 6BIO reduces oxidative stress, improves lipid metabolism, enhances autophagy, and significantly retards liver aging via modulating the GSK-3ß pathway and mTOR pathway. Our findings suggest that 6BIO could be a potential agent to protect the liver in the field of anti-aging pharmacology.

A high-fat diet aggravates osteonecrosis through a macrophage-derived IL-6 pathway.

Inflammation plays an important role in osteonecrosis. Obesity, a risk factor for osteonecrosis, leads to a chronic inflammatory status. We hypothesized that inflammation mediated the effects of obesity on osteonecrosis and tested our hypothesis in a mouse model of osteonecrosis. We fed mice with a high-fat diet (HFD) for 12 weeks before osteonecrosis induction by methylprednisolone and examined bone structure and IL-6 expression. Then we investigated the effects of IL-6 deletion in mice with osteonecrosis on the HFD. Next, we isolated bone marrow cells and determined the cell types responsible for HFD-induced IL-6 secretion. Finally, we investigated the roles of macrophages and macrophage-driven IL-6 in HFD-mediated effects on osteonecrosis and osteogenesis of bone marrow stromal cells (BMSCs). The HFD lead to exacerbated destruction of the femoral head in mice with osteonecrosis and increased IL-6 expression in macrophages. Il-6 knockout or macrophage depletion suppressed the effects of the HFD on bone damage. When co-cultured with macrophages isolated from HFD-fed mice with osteonecrosis, BMSCs showed reduced viability and suppressed osteogenic differentiation. Our results suggest that macrophage-driven IL-6 bridges obesity and osteonecrosis and inhibition of IL-6 or depletion of macrophage may represent a therapeutic strategy for obesity-associated osteonecrosis.

Correction: Lithium-containing biomaterials inhibit osteoclastogenesis of macrophages in vitro and osteolysis in vivo.

Correction for 'Lithium-containing biomaterials inhibit osteoclastogenesis of macrophages in vitro and osteolysis in vivo' by Chenhao Pan et al., J. Mater. Chem. B, 2018, 6, 8115-8126.

Coatings as the useful drug delivery system for the prevention of implant-related infections.

Implant-related infections (IRIs) which led to a large amount of medical expenditure were caused by bacteria and fungi that involve the implants in the operation or in ward. Traditional treatments of IRIs were comprised of repeated radical debridement, replacement of internal fixators, and intravenous antibiotics. It needed a long time and numbers of surgeries to cure, which meant a catastrophe to patients. So how to prevent it was more important than to cure it. As an excellent local release system, coating is a good idea by its local drug infusion and barrier effect on resisting biofilms which were the main cause of IRIs. So in this review, materials used for coatings and evidences of prevention were elaborated.

Puerarin Attenuates Osteoarthritis via Upregulating AMP-Activated Protein Kinase/Proliferator-Activated Receptor-γ Coactivator-1 Signaling Pathway in Osteoarthritis Rats.

BACKGROUND/AIMS: Osteoarthritis is the most common degenerative joint disease and causes major pain and disability in adults. It has been reported that mitochondrial dysfunction in chondrocytes was associated with osteoarthritis. Puerarin has multiple effects including restoring mitochondrial function. In this study, the potential effects of puerarin on osteoarthritis and osteoarthritis associated mitochondrial dysfunctions were evaluated. METHODS: Osteoarthritis rats were treated with puerarin and the severity of osteoarthritis and cartilage damages was evaluated. The mitochondrial biogenesis and functions were analyzed by measuring related proteins expression, mitochondrial DNA content, ATP production, and oxygen consumption. The dependence of AMP-activated protein kinase (AMPK) pathway on puerarin-regulated mitochondrial function was analyzed by applying AMPK inhibitor Compound C. RESULTS: Puerarin treatment alleviated mechanical hyperalgesia and cartilage damage in osteoarthritis rats. Puerarin increased mitochondrial biogenesis and attenuated mitochondrial dysfunctions in osteoarthritis rats. AMPK inhibitor Compound C abolished puerarin's effects. CONCLUSION: Puerarin attenuates osteoarthritis by upregulating the AMPK/proliferator-activated receptor-γ coactivator signaling pathway in osteoarthritis rats.

The quantitative models for broiler chicken response to monochromatic, combined, and mixed light-emitting diode light: A meta-analysis.

Although many experiments have been conducted to clarify the response of broiler chickens to light-emitting diode (LED) light, those published results do not provide a solid scientific basis for quantifying the response of broiler chickens. This study used a meta-analysis to establish light spectral models of broiler chickens. The results indicated that 455 to 495 nm blue LED light produced the greatest positive response in body weight by 10.66% (BW; P < 0.001) and 515 to 560 nm green LED light increased BW by 6.27% (P < 0.001) when compared with white light. Regression showed that the wavelength (455 to 660 nm) was negatively related to BW change of birds, with a decrease of about 4.9% BW for each 100 nm increase in wavelength (P = 0.002). Further analysis suggested that a combination of the two beneficial light sources caused a synergistic effect. BW was further increased in birds transferred either from green LED light to blue LED light (17.23%; P < 0.001) or from blue LED light to green LED light (17.52%; P < 0.001). Moreover, birds raised with a mixture of green and blue LED light showed a greater BW promotion (10.66%; P < 0.001) than those raised with green LED light (6.27%). A subgroup analysis indicated that BW response to monochromatic LED light was significant regardless of the genetic strain, sex, control light sources, light intensity and regime of LED light, environmental temperature, and dietary ME and CP (P > 0.05). However, there was an interaction between the FCR response to monochromatic LED light with those covariant factors (P < 0.05). Additionally, green and yellow LED light played a role in affecting the meat color, quality, and nutrition of broiler chickens. The results indicate that the optimal ratio of green × blue of mixed LED light or shift to green-blue of combined LED light may produce the optimized production performance, whereas the optimal ratio of green/yellow of mixed or combined LED light may result in the optimized meat quality.

Lithium-containing biomaterials inhibit osteoclastogenesis of macrophages in vitro and osteolysis in vivo.

Osteolysis, which is caused by aging, neoplasia, infection, or trauma, is a type of intractable systemic or local syndrome of bone destruction (e.g., peri-implant osteolysis (PIO)). The activation of osteoclasts differentiated from macrophages plays a decisive role in such diseases. To conquer this challenge, herein, a biomaterial capable of inhibiting osteoclastogenesis and osteolysis was designed. Recent research has shown that lithium (Li) can inhibit pro-inflammatory cytokine release in vitro via affecting the pharmacotherapy of psychiatric illnesses. Therefore, we synthesized a pure-phase lithium-calcium-silicate (Li2Ca2Si2O7, LCS) bioceramic and further prepared extracts to assess the effect of LCS on RANKL-induced osteoclastogenesis in vitro and Ti particle-induced osteolysis in vivo as well as the corresponding mechanism. The results demonstrated that LCS inhibited RANKL-induced osteoclastogenesis of macrophages, bone resorption area, and F-actin ring formation in a dose-dependent manner. The mechanism is related to the suppression of the NF-kB signaling pathways mediating the inhibitory effects of LCS. Moreover, LCS was found to be able to inhibit calvarial osteolysis in a mouse model through micro-CT and histological analysis. These findings suggest that LCS may be a promising biomaterial for suppressing osteolysis, thus paving the way for the treatment of osteoporosis using bioactive inorganic materials.

20(S)-Protopanaxadiol Inhibits Titanium Particle-Induced Inflammatory Osteolysis and RANKL-Mediated Osteoclastogenesis via MAPK and NF-κB Signaling Pathways.

Osteolysis is a principal reason for arthroplasty failure like aseptic loosening induced by Titanium (Ti) particle. It is a challenge for orthopedic surgeons. Recent researches show that 20(S)-protopanaxadiol can inhibit inflammatory cytokine release in vitro. This study aims to assess the effect of 20(S)-protopanaxadiol on Ti particle-induced osteolysis and RANKL-mediated osteoclastogenesis. Micro-CT and histological analysis in vivo indicated the inhibitory effects of 20(S)-protopanaxadiol on osteoclastogenesis and the excretion of inflammatory cytokines. Next, we demonstrated that 20(S)-protopanaxadiol inhibited osteoclast differentiation, bone resorption area, and F-actin ring formation in a dose-dependent manner. Moreover, mechanistic studies suggested that the suppression of MAPK and NF-κB signaling pathways were found to mediate the inhibitory effects of 20(S)-protopanaxadiol. In conclusion, 20(S)-protopanaxadiol may suppress osteoclastogenesis in a dose- dependent manner and it could be a potential treatment of Ti particle-induced osteolysis.