Innervate Commercial Fabrics with Spirally-Layered Iontronic Fibrous Sensors Toward Dual-Functional Smart Garments.

Electronic fabrics exhibit desirable breathability, wearing comfort, and easy integration with garments. However, surficial deposition of electronically functional materials/compounds onto fabric substrates would consequentially alter their intrinsic properties (e.g., softness, permeability, biocompatibility, etc.). To address this issue, here, a strategy to innervate arbitrary commercial fabrics with unique spirally-layered iontronic fibrous (SLIF) sensors is presented to realize both mechanical and thermal sensing functionalities without sacrificing the intrinsic fabric properties. The mechanical sensing function is realized via mechanically regulating the interfacial ionic supercapacitance between two perpendicular SLIF sensors, while the thermal sensing function is achieved based on thermally modulating the intrinsic ionic impedance in a single SLIF sensor. The resultant SLIF sensor-innervated electronic fabrics exhibit high mechanical sensitivity of 81 N-1, superior thermal sensitivity of 34,400 Ω °C-1, and more importantly, greatly minimized mutual interference between the two sensing functions. As demonstrations, various smart garments are developed for the precise monitoring of diverse human physiological signals. Moreover, artificial intelligence-assisted object recognition with high-accuracy (97.8%) is demonstrated with a SLIF sensor-innervated smart glove. This work opens up a new path toward the facile construction of versatile smart garments for wearable healthcare, human-machine interfaces, and the Internet of Things.

Molecular mechanism of RBM14-mediated promotion of proliferation, migration, and invasion in osteosarcoma.

Background: Osteosarcoma (OS) is an exceptionally aggressive bone neoplasm that predominantly impacts the paediatric and adolescent population, exhibiting unfavourable prognosis. The importance of RNA binding motif protein 14 (RBM14) in the aetiology of OS is not well understood, despite its established involvement in several other types of cancer. Methods: In this study, we conducted an analysis of the expression profiles of RBM14 in cancer tissues and cell lines. To achieve this, we will utilised data obtained from various databases including The Cancer Genome Atlas Program (TCGA) project, The Genotype-Tissue Expression (GTEx) Project, Gene Expression Omnibus (GEO) database, and cancer cell line encyclopedia (CCLE) data. Furthermore, this study also aims to examine the effects of RBM14 on the proliferation, migration, and invasive properties of OS cells using cell functional gain and loss studies. In this study, we carried out an in-depth investigation to explore possible molecular pathways that underlie the regulation of the malignant phenotype found in OS by RBM14. This investigation involved integrating data from RBM14 overexpression, RBM14 knockdown RNA-seq experiments, and an array comprising 6,096 perturbed genes obtained from the Genetic Perturbation Similarity Analysis Database (GPSAdb). This research offers an opportunity to build a robust conceptual framework for the potential advancement of novel therapeutic approaches that are especially aimed at attacking OS. Results: RBM14 plays an active role in OS by significantly contributing to the enhancement of cellular proliferation, migration, and invasion. At the molecular level, it is probable that RBM14 exerts control over the malignant characteristics of OS through its modulation of the Hippo signalling system. Conclusions: The above-mentioned findings underscore the significant importance of RBM14 as an intriguing target for therapy for the mitigation and management of OS. This particular protein holds an excellent opportunity for the development of novel and efficacious therapeutic approaches that possess the potential to yield favorable results for patients affected with OS.

Functional role of P2X7 purinergic receptor in cancer and cancer-related pain.

Numerous studies have revealed that the ATP-gated ion channel purinergic 2X7 receptor (P2X7R) plays an important role in tumor progression and the pathogenesis of cancer pain. P2X7R requires activation by extracellular ATP to perform its regulatory role functions. During tumor development or cancer-induced pain, ATP is released from tumor cells or other cells in the tumor microenvironment (such as tumor-associated immune cells), which activates P2X7R, opens ion channels on the cell membrane, affects intracellular molecular metabolism, and regulates the activity of tumor cells. Furthermore, peripheral organs and receptors can be damaged during tumor progression, and P2X7R expression in nerve cells (such as microglia) is significantly upregulated, enhancing sensory afferent information, sensitizing the central nervous system, and inducing or exacerbating pain. These findings reveal that the ATP-P2X7R signaling axis plays a key regulatory role in the pathogenesis of tumors and cancer pain and also has a therapeutic role. Accordingly, in this study, we explored the role of P2X7R in tumors and cancer pain, discussed the pharmacological properties of inhibiting P2X7R activity (such as the use of antagonists) or blocking its expression in the treatment of tumor and cancer pain, and provided an important evidence for the treatment of both in the future.

Kurarinone, a flavonoid from Radix Sophorae Flavescentis, inhibits RANKL-induced osteoclastogenesis in mouse bone marrow-derived monocyte/macrophages.

Inflammation-induced osteoclast proliferation is a crucial contributor to impaired bone metabolism. Kurarinone (KR), a flavonoid extracted from the Radix Sophorae Flavescentis, exhibits notable anti-inflammatory properties. Nevertheless, the precise influence of KR on osteoclast formation remains unclear. This study's objective was to assess the impact of KR on osteoclast activity in vitro and unravel its underlying mechanism. Initially, a target network for KR-osteoclastogenesis-osteoporosis was constructed using network pharmacology. Subsequently, the intersecting targets were identified through the Venny platform and a PPI network was created using Cytoscape 3.9.1. Key targets within the network were identified employing topological algorithms. GO enrichment and KEGG pathway analysis were then performed on these targets to explore their specific functions and pathways. Additionally, molecular docking of potential core targets of KR was conducted, and the results were validated through cell experiments. A total of 83 target genes overlapped between KR and osteoclastogenesis-osteoporosis targets. Enrichment analysis revealed their role in inflammatory response, protein tyrosine kinase activity, osteoclast differentiation, and MAPK and NF-κB signaling pathways. PPI analysis and molecular docking demonstrate that key targets MAPK14 and MAPK8 exhibit more stable binding with KR compared to other proteins. In vitro experiments demonstrate that KR effectively inhibits osteoclast differentiation and bone resorption without cellular toxicity. It suppresses key osteoclast genes (NFATc1, c-Fos, TRAP, MMP9, Ctsk, Atp6v2), hinders IκB-α degradation, and inhibits ERK and JNK phosphorylation, while not affecting p38 phosphorylation. The results indicate that KR may inhibit osteoclast maturation and bone resorption by blocking NF-κB and MAPK signaling pathways, suggesting its potential as a natural therapeutic agent for osteoporosis.

Network Pharmacology and Experimental Validation to Elucidate the Pharmacological Mechanisms of Luteolin Against Chondrocyte Senescence.

BACKGROUND: Luteolin, a flavonoid found in various medicinal plants, has shown promising antioxidant, anti-inflammatory, and anti-aging properties. The cartilaginous endplate (CEP) represents a crucial constituent of the intervertebral disc (IVD), assuming a pivotal responsibility in upholding both the structural and functional stability of the IVD. OBJECTIVE: Exploring the precise mechanism underlying the protective effects of luteolin against senescence and degeneration of endplate chondrocytes (EPCs). METHODS: Relevant targets associated with luteolin and aging were obtained from publicly available databases. To ascertain cellular functions and signaling pathways, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were employed. Core genes were identified through the construction of a protein-protein interaction (PPI) network. Molecular docking (MD) was utilized to assess the binding affinity of luteolin to these core genes. Finally, the impact of luteolin on the senescence and degeneration of EPCs was evaluated in an in vitro cellular senescence model induced by tert-butyl hydroperoxide (TBHP). RESULTS: There are 145 overlapping targets between luteolin and senescence. Analysis using GO revealed that these targets primarily participate in cellular response to oxidative stress and reactive oxygen species. KEGG analysis demonstrated that these markers mainly associate with signaling pathways such as p53 and PI3K-Akt. MD simulations exhibited luteolin's binding affinity to P53, Cyclin-dependent kinase (CDK)2, and CDK4. Cell cycle, cell proliferation, and ß- galactosidase assays confirmed that luteolin mitigated senescence in SW1353 cells. Western blot assays exhibited that luteolin significantly suppressed the expression of Matrix Metallopeptidase (MMP) 13, P53, and P21, while concurrently promoting CDK2, CDK4, and Collagen Type II Alpha 1 (COL2A1) expression. CONCLUSION: In summary, luteolin demonstrated beneficial properties against aging and degeneration in EPCs, offering novel insights to mitigate the progression of intervertebral disc degeneration (IVDD).

ATG9A as a potential diagnostic marker of intervertebral disc degeneration: Inferences from experiments and bioinformatics analysis incorporating sc-RNA-seq data.

BACKGROUND: Disfunctional autophagy plays a pivotal role in Intervertebral Disc Degeneration (IDD) progression. however, the connection between Autophagy-related gene 9A (ATG9A) and IDD has not been reported. METHODS: Firstly, transcriptome datasets from the GEO and Autophagy-related genes (ARGs) from GeneCards were carried out using R. Following this, IDD-specific signature genes were identified through methods such as least absolute shrinkage and selection operator (LASSO), random forest (RF), and support vector machine (SVM) analyses. Validation of these findings proceeded through in vitro experiments, evaluation of independent datasets, and analysis of receiver operating characteristic (ROC) curves. Subsequent steps incorporated co-expression analysis, Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, Gene Set Enrichment Analysis (GSEA), and construction of competing endogenous RNA (ceRNA) network. The final section established the correlation between immune cell infiltration, ATG9A, and IDD utilizing the CIBERSORT algorithm and single-cell RNA (scRNA) sequencing data. RESULTS: Research identified 87 differentially expressed genes, with only ATG9A noted as an IDD signature gene. Analysis of in vitro experiments and independent datasets uncovered a decrease in ATG9A expression within the degeneration group. The area under the curve (AUC) of ATG9A exceeded 0.8 following ROC analysis. Furthermore, immune cell infiltration and scRNA sequencing data analysis elucidated the substantial role of immune cells in IDD progression. A ceRNA network was constructed, centered around ATG9A, included 4 miRNAs and 22 lncRNAs. CONCLUSION: ATG9A was identified as a diagnostic gene for IDD, indicating its viability as a effective target for therapy disease.

P2 purinergic receptors regulate the progression of colorectal cancer.

More and more studies have revealed that P2 purinergic receptors play a key role in the progression of colorectal cancer (CRC). P2X and P2Y purinergic receptors can be used as promoters and regulators of CRC and play a dual role in the progression of CRC. CRC microenvironment is rich in ATP and its cleavage products (ADP, AMP, Ado), which act as activators of P2X and P2Y purinergic receptors. The activation of P2X and P2Y purinergic receptors regulates the progression of CRC mainly by regulating the function of immune cells and mediating different signal pathways. In this paper, we focus on the specific mechanisms and functional roles of P2X7, P2Y12, and P2Y2 receptors in the growth and progression of CRC. The antagonistic effects of these selective antagonists of P2X purinergic receptors on the growth, invasion, and metastasis of CRC were further discussed. Moreover, different studies have reported that P2X7 receptor can be used as an effective predictor of patients with CRC. All these indicate that P2 purinergic receptors are a key regulator of CRC. Therefore, antagonizing P2 purinergic receptors may be an innovative treatment for CRC.

The Clinical Efficacy of Autologous Platelet-Rich Plasma Interventional Circulatory Perfusion Combined with Radiofrequency Ablation and Thermocoagulation in the Treatment of Discogenic Low Back Pain.

Objective: In this study, we aimed to explore the efficacy of the autologous platelet-rich plasma (PRP) interventional circulatory perfusion combined with radiofrequency ablation and thermocoagulation (RFAT) in the treatment of discogenic low back pain (DLBP). Methods: From January 2020 to November 2022, 158 patients of the Second Affiliated Hospital of Nanchang University were selected as the study subjects, and 24 patients met the exclusion criteria. The 134 patients who met the inclusion criteria were divided into 65 patients in the control group (3 patients lost to follow-up) and 69 patients in the observation group (5 patients lost to follow-up), so 126 patients were actually completed the study, including 62 patients in the control group and 64 patients in the observation group. The control group responsible disc received RFAT, and an interventional circulatory perfusion was performed; the observation group received RFAT, and an interventional circulatory perfusion was performed, and then autologous PRP 2 ml was injected. Visual Analog Scale (VAS) and Oswestry Disability Index (ODI) were performed before and 4 and 8 weeks after treatment, and the efficacy was evaluated at 4 and 8 weeks after treatment. The changes of lumbar disc MRI before and after treatment were observed. Results: The differences in the Visual Analog Scale (VAS) scores and the Oswestry Disability Index (ODI) between the observation group and the control group before the treatment were not statistically significant (P > 0.05 in both). However, four weeks and eight weeks after the treatment, the VAS scores and the ODIs were significantly lower in both groups than those before the treatment (P < 0.05 in both). In terms of the therapeutic efficacy, eight weeks after the treatment, the total effective rates in the control group and the observation group were 67.7% and 87.5%, respectively, with the observation group being superior to the control group (P < 0.05). Conclusion: After RFAT, interventional circulatory perfusion combined with autologous PRP intramedullary injection in the lumbar disc is a safe and effective treatment for DLBP, and it had superior long-term effects in improving the clinical symptoms and patient dysfunction than the RFAT and interventional circulatory perfusion.

The Correlation of Global Spinal Realignment With the Quality of Life After Corrective Surgery for Delayed Thoracolumbar Osteoporotic Fracture-Related Kyphosis.

BACKGROUND AND OBJECTIVES: Few studies have been conducted to evaluate the precise impact of corrective surgery on sagittal spinal realignment and clinical outcomes in cases of delayed thoracolumbar osteoporotic fracture-related kyphosis. To assess the efficacy of corrective surgery on sagittal spinal alignment and investigate the relationship between spinal alignment and health-related quality of life (HRQoL) in patients with delayed thoracolumbar osteoporotic fracture-related kyphosis. METHODS: A total of 78 patients were enrolled. The characteristics and surgical variables were meticulously documented. The sagittal spinal parameters were measured, and the HRQoL was evaluated using Oswestry Disability Index (ODI), SF-12 Physical Component Score (SF-12 PCS), and Scoliosis Research Society-22 Patient Questionnaire (SRS-22) before and after surgery. The changes in spinal parameters and HRQoL were analyzed through the paired t -test. The Pearson correlation analysis was performed to analyze the correlation of parameters with HRQoL. Then, a multiple stepwise regression analysis was performed with HRQoL scores as the dependent variable and spinal parameters as the independent variable. RESULTS: The operative time was 185.9 ± 33.2 min, and the estimated blood loss was 782.8 ± 145.2 mL. The results of the paired t -test revealed a significant difference preoperatively and at the final follow-up in the thoracic kyphosis, thoracolumbar kyphosis (TLK), lumbar lordosis, T9 tilt, pelvic tilt, sacral slope, sagittal vertical axis, and spinosacral angle as well as the ODI, SF-12 PCS, and SRS-22 ( P < .05). Multiple stepwise regression analysis revealed that TLK and pelvic tilt, TLK and sagittal vertical axis, and TLK were the primary parameters affecting the ODI, SF-12 PCS, and SRS-22, respectively. CONCLUSION: Corrective surgery can effectively realign the global spine and improve HRQoL in patients with delayed thoracolumbar osteoporotic fracture-related kyphosis. The change of TLK is a driving factor to realign the global spine.

Improvement of pulmonary function and reconstructed 3D lung volume after deformity correction for thoracic spinal posttubercular kyphosis: a multicenter study.

OBJECTIVE: The aim of this study was to investigate the influence of corrective surgery on thoracic spinal posttubercular kyphosis (PTK) with respect to lung volume and pulmonary function. METHODS: This was a retrospective study of 126 patients (72 males and 54 females) who underwent posterior vertebral column resection (PVCR) for severe thoracic spinal PTK between September 2013 and June 2020. The patients' spinal parameters, results of their pulmonary function test (PFT), and CT-based 3D lung volume were recorded and analyzed preoperatively and at final follow-up. The correlation of kyphosis correction with the PFT and lung volume was evaluated. RESULTS: The mean local kyphosis decreased from 112.5° to 37.2°, and the mean local scoliosis decreased from 20.9° to 5.2°; C2-7 lordosis, thoracic kyphosis, and lumbar lordosis also significantly improved after surgery. The mean CT-based lung volume significantly increased from 2.9 L preoperatively to 3.6 L at the final follow-up. The indices of PFT, including forced vital capacity (FVC), percent predicted FVC, total lung capacity, and forced expiratory volume in 1 second, were also significantly improved, and 60 patients with pulmonary dysfunction recovered to normal at the final follow-up. The correlation analysis revealed that the correction of local kyphosis was closely correlated with the improvement in PFT and the increase in lung volume. CONCLUSIONS: PVCR cannot only effectively realign the spine in patients with severe thoracic spinal PTK deformity but also significantly improve pulmonary function. Adequate local kyphosis correction should be highly valued, as it is a key factor in increasing lung volume.

Contribution of P2X purinergic receptor in cerebral ischemia injury.

The development of cerebral ischemia involves brain damage and abnormal changes in brain function, which can cause neurosensory and motor dysfunction, and bring serious consequences to patients. P2X purinergic receptors are expressed in nerve cells and immune cells, and are mainly expressed in microglia. The P2X4 and P2X7 receptors in the P2X purinergic receptors play a significant role in regulating the activity of microglia. Moreover, ATP-P2X purine information transmission is involved in the progression of neurological diseases, including the release of pro-inflammatory factors, driving factors and cytokines after cerebral ischemia injury, inducing inflammation, and aggravating cerebral ischemia injury. P2X receptors activation can mediate the information exchange between microglia and neurons, induce neuronal apoptosis, and aggravate neurological dysfunction after cerebral ischemia. However, inhibiting the activation of P2X receptors, reducing their expression, inhibiting the activation of microglia, and has the effect of protecting nerve function. In this paper, we discussed the relationship between P2X receptors and nervous system function and the role of microglia activation inducing cerebral ischemia injury. Additionally, we explored the potential role of P2X receptors in the progression of cerebral ischemic injury and their potential pharmacological targets for the treatment of cerebral ischemic injury.

Exosomal miR-335 derived from mature dendritic cells enhanced mesenchymal stem cell-mediated bone regeneration of bone defects in athymic rats.

BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BM-MSCs) embedded in a bio-compatible matrix has been demonstrated as a promising strategy for the treatment of bone defects. This study was designed to explore the effect and mechanism of exosomes derived from mature dendritic cells (mDC-Exo) on the BM-MSCs-mediated bone regeneration using the matrix support in an athymic rat model of femoral bone defect. METHODS: The BM-MSCs were isolated from rats and incubated with osteoblast induction medium, exosomes derived from immature DCs (imDC-Exo), mDC-Exo, and miR-335-deficient mDC-Exo. BM-MSCs treated without or with mDC-Exo were embedded in a bio-compatible matrix (Orthoss®) and then implanted into the femoral bone defect of athymic rats. RESULTS: mDC-Exo promoted the proliferation and osteogenic differentiation of BM-MSCs by transferring miR-335. Mechanistically, exosomal miR-335 inhibited Hippo signaling by targeting large tongue suppressor kinase 1 (LATS1) and thus promoted the proliferation and osteogenic differentiation of BM-MSCs. Animal experiments showed that mDC-Exo enhanced BM-MSCs-mediated bone regeneration after bone defect, and this effect was abrogated when miR-335 expression was inhibited in mDC-Exo. CONCLUSION: mDC-Exo promoted osteogenic differentiation of BM-MSCs and enhanced BM-MSCs-mediated bone regeneration after femoral bone defect in athymic rats by transferring miR-335.

A rapid resistance measurement system for quartz pendulums.

A quartz pendulum, gold plated on both sides, is the core component of a quartz accelerometer. Currently, a two-wire manual measurement method is employed to measure the resistance at 24 key positions on the gold plating to evaluate manufacturing quality. This method is time-consuming and has poor repeatability. In this paper, an automatic measurement system is proposed to measure these 24 resistances. The proposed system consists primarily of a lab-designed holder that clamps the sample, a machine vision unit to measure the sample position, RXY-stages for precise positioning, two lab-designed probes with 48 needles to sense the electrical signals, a multichannel self-switching module to sample the electrical signals from the probe needles, and a 7½-digital multimeter to measure the resistances. In addition, a simple, precise pre-measurement positioning method is introduced here. Experimental results show that the quartz-pendulum resistances can be measured quickly and precisely using the proposed system. The measurement rate of 1 pendulum/min is a factor of 10 faster than the current manual method, the measurement stability error is only 0.9 mΩ (a relative error of 0.13%), and the measurement repeatability error is 1.2 mΩ (a relative error of 0.20%).

Silencing of long noncoding RNA SBF2-AS1 inhibits proliferation, migration and invasion and contributes to apoptosis in osteosarcoma cells by upregulating microRNA-30a to suppress FOXA1 expression.

Objectives: Long noncoding RNA (lncRNA) SBF2-AS1 was found to be related to some tumors. Nevertheless, the role of SBF2-AS1 in osteosarcoma (OS) is still needed to be elaborated. This study is conducted to examine the expression of lncRNA SBF2-AS1 in OS with the involvement of microRNA-30a (miR-30a) and FOXA1. Methods: OS tissues and its corresponding adjacent normal tissues were obtained for the detection of SBF2-AS1 expression and its relations with clinical phenotypes. OS cells with most significant expression of SBF2-AS1 were selected for subsequent experiments. Moreover, a series of experiments were performed to detect proliferation, invasion, migration, colony formation, cell cycle distribution and apoptosis of OS cells. Furthermore, the binding site between SBF2-AS1 and miR-30a as well as between miR-30a and FOXA1 was verified. Results: SBF2-AS1 was overexpressed in tissues and cells of OS. Additionally, silencing of SBF2-AS1 and miR-30a overexpression inhibited the proliferation, migration and invasion of OS cells and promoted their apoptosis. Moreover, lncRNA SBF2-AS1 regulated miR-30a by serving as a ceRNA, thus promoting FOXA1 expression. Furthermore, interfered SBF2-AS1 or upregulated miR-30a restrained the growth of OS. Conclusion: Our study confirms that silencing of SBF2-AS1 represses proliferation, migration and invasion of OS cells and promotes their apoptosis by binding to miR-30a and inhibiting FOXA1 expression.

Analysis of anti-osteoporosis function of chlorogenic acid by gene microarray profiling in ovariectomy rat model.

The aim of the present study was to clarify the effect of chlorogenic acid (CGA) on estrogen deficiency-induced osteoporosis based on micro-computed tomography (micro-CT) and potential mechanism of gene regulation via microarray profiling. Eighteen female Sprague-Dawley rats were divided randomly into sham-operated group, ovariectomy (OVX) plus saline vehicle group, and OVX plus CGA treatment group (CGA at 45 mg/kg/day). The loss of bone mass of the femoral metaphysis was evaluated by micro-CT to represent. Gene expression profiling was analyzed for bone marrow mesenchymal stem cells (BMSCs) of OVX and OVXT groups. Bioinformatics analysis was used to find the potential pathways regulated by CGA. OVX-induced osteoporosis could decrease femur bone mineral density (BMD), bone volume/tissue volume (BV/TV), trabecula number (Tb.N), and trabecular thickness (Tb.Th) and increased the trabecular separation (Tb.Sp) and structure model index (SMI) in the rats. Gene microarray profiling showed 121 differentially expressed genes in collected BMSCs between OVX and OVXT groups were identified with a threshold of a two-fold change and P<0.05. Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to analyze the potential mechanism of CGA and we observed that many mitogen-activated protein kinase (MAPK) pathway associtated genes were altered, suggesting this pathway may play an important role. CGA improved bone quality by modifying the BMD and trabecular microarchitecture. Differential expression genes were screened by gene microarray profile and the results suggested MAPK pathway might participate in the process of OVX-induced bone remodeling.

Quercetin rescued TNF-alpha-induced impairments in bone marrow-derived mesenchymal stem cell osteogenesis and improved osteoporosis in rats.

To investigate the effect of quercetin on promoting the proliferation of bone marrow mesenchymal stem cells (BMSCs) and improving osteoporosis in rats. Rats were randomly divided into the sham, OVX and quercetin+OVX groups. In the sham and OVX groups, rats were given carboxymethyl cellulose sodium (CMC-Na). In the quercetin+OVX group, rats were given quercetin (50 mg/kg) once a day. Eight weeks after rats were treated, femurs were subjected to micro-CT scans, and bone biomechanical properties were analysed by the three-point flexural test. In addition, BMSCs were isolated and characterised by MTT, RT-PCR and Western blot analysis. In vivo, quercetin increased bone mineral density (BMD) and improved bone biomechanical properties in postmenopausal osteoporosis rat models. In vitro, TNF-α led to the activation of nuclear factor-kappa B (NF-κB) and the degradation of ß-catenin, which were significantly inhibited by quercetin. Furthermore, quercetin promoted BMSC proliferation and osteogenic differentiation. In conclusion, quercetin improved in vitro models of osteoporosis and protected against TNF-α-induced impairments in BMSC osteogenesis.

Shp2 regulates chlorogenic acid-induced proliferation and adipogenic differentiation of bone marrow-derived mesenchymal stem cells in adipogenesis.

Chlorogenic acid (CGA) exhibits various biological properties, including the inhibition of oxidation, obesity, apoptosis and tumorigenesis. CGA is also able to promote cell survival and proliferation. The aim of the present study was to determine the effects and underlying molecular mechanisms of CGA on the adipogenesis of bone marrow­derived mesenchymal stem cells (BMSCs). Treatment with CGA had a marginal effect on cell proliferation, by promoting the expression levels of phosphorylated Akt and cyclin D1. Furthermore, treatment with CGA also upregulated the phosphorylation of extracellular signal­regulated kinase (Erk) and inhibited the adipocyte differentiation of BMSCs by inhibiting the expression of peroxisome proliferator­activated receptor (PPAR)γ and CCAAT/enhancer binding protein (C/EBP)α. However, knockdown of the expression of Shp2 attenuated CGA­induced proliferation and inhibited the phosphorylation of Akt and expression of cyclin D1. Furthermore, CGA treatment upregulated Erk phosphorylation and decreased the expression levels of PPARγ and CEBPα, which was inhibited by treatment with the Shp2 PTPase activity inhibitor, NSC­87877. The results of the present study suggested that CGA­induced Akt and Erk pathways regulate proliferation and differentiation and that Shp2 is important in the proliferation and differentiation of BMSCs.