Human MMP13 ELISA kit
- Known as:
- Human MMP13 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50677
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Human MMP13 ELISA kit
Related genes to: Human MMP13 ELISA kit
- Gene:
- MMP13 NIH gene
- Name:
- matrix metallopeptidase 13
- Previous symbol:
- -
- Synonyms:
- CLG3
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-20
- Date modifiied:
- 2016-10-05
Related products to: Human MMP13 ELISA kit
Related articles to: Human MMP13 ELISA kit
- Tongbi Lingding (TBLD) has demonstrated therapeutic effects in early- and mid-stage osteoarthritis (OA), but its active components and underlying mechanisms remain unclear. This study aimed to identify the bioactive compounds of TBLD and explore the potential molecular mechanisms underlying its therapeutic effects against OA. A destabilization of the medial meniscus (DMM)-induced OA mouse model and IL-1β-stimulated chondrocytes were used to evaluate the therapeutic effects of TBLD. Ultra-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) was performed to identify TBLD-associated compounds in blood and knee joints. Network pharmacology, transcriptomic analysis, molecular docking, and in vitro experiments were integrated to investigate the potential mechanisms underlying the effects of TBLD. TBLD markedly alleviated cartilage degeneration and subchondral bone sclerosis in OA mice. UPLC-MS/MS identified 2295 compounds, among which 178 and 102 TBLD-associated compounds were detected in blood and knee joints, respectively. Seventy-six compounds with predicted targets and 153 shared targets were identified. Functional enrichment analysis indicated that these targets were mainly associated with the NOD-like receptor (NLR) and NF-κB signaling pathways. Molecular docking predicted potential interactions between key compounds and NLRP3 and p65. Furthermore, hinokiflavone and dehydroabietic acid suppressed inflammatory responses, restored extracellular matrix metabolism, and inhibited IL-1β-induced MMP3 and MMP13 expression in chondrocytes. Hinokiflavone treatment also reduced the expression of NLRP3 inflammasome-related proteins and attenuated the phosphorylation of NF-κB signaling-related proteins in TNF-α-stimulated chondrocytes. TBLD exerts protective effects against OA that may be associated with changes in NLRP3/NF-κB-related inflammatory signaling, further supporting its potential therapeutic application in OA. - Source: PubMed
Publication date: 2026/09/19
Zhang ZhenzhenWang JinhuiBian HuihuiChen JiangpingWang JiaminSun YongGao ZhiminSu LiLiu YingLiang Yi - Post-traumatic osteoarthritis (PTOA) is a progressive joint disease characterised by cartilage degeneration and subchondral bone remodelling, in which persistent oxidative stress and inflammation jointly drive structural deterioration and functional loss. Most therapeutic strategies primarily alleviate symptoms or target single tissues, with limited efficacy in modifying disease progression. Here, we developed degradable ultrathin iron sulphide nanosheets (FeSNSs) and prepared a PEGylated therapeutic formulation (FeS-PEG) that concurrently protects articular cartilage and stabilises subchondral bone by alleviating oxidative-stress-associated joint damage in PTOA. The resulting FeS-PEG formulation exhibited favourable colloidal stability and pronounced ROS-scavenging activity. In vitro, FeS-PEG reduced intracellular ROS and lipid peroxidation in HO- and IL-1β-stimulated chondrocytes, restored antioxidant enzyme activity, attenuated COX-2/iNOS and pro-inflammatory cytokine expression, and preserved chondrocyte phenotype by promoting COL II expression while suppressing MMP3- and MMP13-mediated matrix degradation. Transcriptomic profiling further revealed that FeS-PEG reprogrammed IL-1β-induced PTOA-like gene expression, rebalancing extracellular matrix organisation, inflammatory signalling, and redox homeostasis. In an anterior cruciate ligament transection-induced PTOA rat model, intra-articular FeS-PEG administration significantly reduced cartilage erosion, OARSI histological scores, and local inflammation. Micro-CT revealed preserved subchondral bone microarchitecture with increased bone volume fraction and decreased trabecular separation, indicating inhibition of early maladaptive bone remodelling. Collectively, the findings establish FeS-PEG as a dual-functional, ROS-targeting nanotherapeutic platform that couples cartilage protection with subchondral bone preservation, offering a promising disease-modifying strategy for PTOA and broadening the potential applications of FeS-based nanomedicine in orthopaedics. - Source: PubMed
Publication date: 2026/09/01
Xu JiajunWang WenboLiu LiWang ChenglongLiu NanWang XiaomeiLi LianxinDong Jinlei - Chondrocytes and mesenchymal stromal cells (MSC) metabolism shapes cartilage matrix quality, but cartilage engineering lacks a non-destructive, time-resolved readout that links oxygen uses to matrix assembly and mechanics under standard culture conditions. We continuously recorded oxygen-consumption rate (OCR) in nasal chondrocyte (NC), MSC, and NC-MSC co-culture pellets cultured for 27 days under normoxia, and integrated OCR trajectories with time-resolved gene expression, matrix histology, glycosaminoglycan (GAG)/DNA, and unconfined compression mechanics across defined NC:MSC ratios (monocultures; 3:1, 2:1, 1:1, 1:2, 1:3). OCR trajectories were reproducibly tri-phasic-(I) condensation/priming (Days 0-9), (II) differentiation/matrix synthesis (Days 9-21/24), and (III) maturation/remodeling (Days 24-27)-and strongly composition dependent. NC-rich mixtures exhibited an earlier hypoxic tone with transient HIF-1α, accelerated SOX9 followed by ACAN and COL2A1 induction, and marked GAG synergy peaking at 3:1. MSC-rich mixtures sustained late respiration with higher PGC-1α, elevated COL10A1 and MMP13, and achieved the highest equilibrium modulus at 1:3 despite lower GAG/DNA. An OCR downshift near Day 24 marked metabolic settling in most groups, whereas 1:3 pellets maintained or increased respiration, consistent with continued oxidative remodeling. Correlation analyses linked OCR features to hyaline anabolism in NC-rich pellets and to remodeling/hypertrophy in MSC-rich pellets, indicating ratio-specific coordination between respiratory and matrix-associated signatures. These findings support OCR monitoring as a sensitive, non-destructive process metric associated with chondrogenic stage transitions, provide guidance for selecting NC-rich ratios to maximize hyaline fidelity and GAG productivity, and MSC-rich ratios to increase stiffness while managing hypertrophic risk, and offer a generalizable framework for in-process bioenergetic control across tissue-engineering contexts. - Source: PubMed
Ma ZhiyaoMcEachern LiamLan XiaoyiLi David XinzheyangAnsari Aahil AAu IvanBarker MadelineKunze MelanieMulet-Sierra AilletteAdesida Adetola B - Osteoarthritis (OA) is a chronic degenerative joint disease characterized by progressive articular cartilage degradation. Punicic acid (PA), a plant-derived n-3 polyunsaturated fatty acid, has been reported to exert anti-inflammatory and anti-apoptotic effects. However, the molecular mechanisms underlying its effects in OA remain incompletely understood. In this study, bioinformatics analysis was performed to identify apoptosis-related differentially expressed genes (DEGs) and enriched signaling pathways associated with OA. An in vitro OA-like model was established using interleukin-1β (IL-1β)-stimulated SW1353 cells, which were subsequently treated with different concentrations of PA. PA suppressed IL-1β-induced expression of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), matrix metalloproteinase-3 (MMP-3),matrix metalloproteinase-13 (MMP-13), and A Disintegrin And Metalloproteinase with Thrombospondin Motifs 5 (ADAMTS-5) and attenuated apoptosis by modulating Bcl-2-associated X protein (BAX) and B-cell lymphoma 2 (BCL-2) expression. Notably, target prediction and dual-luciferase reporter assays confirmed that mitogen-activated protein kinase kinase 6 (MAP2K6) is a direct target of microRNA-29a-3p (miR-29a-3p), and PA increased miR-29a-3p expression in the in vitro OA-like model. Furthermore, PA inhibited MAP2K6-mediated activation of the p38 mitogen-activated protein kinase (p38 MAPK) pathway, thereby attenuating downstream inflammatory and apoptotic signaling. These findings suggest that PA exerts chondroprotective effects by modulating the miR-29a-3p/MAP2K6/p38 MAPK signaling axis, highlighting its therapeutic potential and supporting the development of miRNA-based therapeutic strategies for OA. - Source: PubMed
Publication date: 2026/09/16
Wang WeiZhang TaoYu ChaoXu Zhi-XiongLuo LongDong LiangXu Wen-Sheng - Osteoarthritis (OA) is a chronic and progressive joint disorder characterized by persistent inflammation, extracellular matrix (ECM) disruption, and chondrocyte apoptosis. This study aimed to investigate the protective effects of ginsenoside Rg3 (Rg3), a natural steroidal saponin from , on OA and to elucidate its underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/09/15
Lu XinjianWang ZhaoyangHu WeifengHu JiongZou Yang