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
- Intervertebral disc degeneration (IVDD) contributes to persistent low back pain, but existing treatments focus on symptom relief rather than addressing the degeneration. Notoginsenoside R1 (NR1), a bioactive saponin derived from Panax notoginseng, has exhibited protective effects in experimental models of disc injury. However, its clinical application is limited by poor bioavailability and rapid clearance. Here, NR1 was encapsulated into poly(lactic-co-glycolic acid) nanoparticles (NR1@PLGA) to improve local drug retention. NR1@PLGA showed uniform particle characteristics, prolonged NR1 release, and time-dependent uptake by nucleus pulposus cells (NPCs). Under HO-induced oxidative stress, NR1@PLGA reduced SA-β-gal-positive cells, preserved aggrecan and collagen II (Col-2) expression, and improved cell viability compared with free NR1 at the same concentration. In a rat caudal puncture model, intradiscal administration of NR1@PLGA preserved T2-weighted MRI signals, improved histological outcomes, increased aggrecan expression, and decreased MMP-13 levels. No obvious abnormalities were observed in major organs or serum biochemical indicators related to liver and kidney function during the 4-week observation period. These results demonstrate that NR1@PLGA is a potential treatment for IVDD, with PLGA encapsulation enhancing the efficacy of NR1. - Source: PubMed
Zheng BaichuanZhong HaotianWang ZhengweiQin JunyuXie ZiyingTang RongHu ChengshangZhang XiumingLi JianwenLi Songbo - Stroke remains a leading cause of global mortality and long-term disability. Despite the clinical success of reperfusion therapies, their efficacy is hampered by narrow therapeutic windows and the risk of secondary brain injury. Matrix metalloproteinases (MMPs), a family of zinc-dependent endopeptidases, have emerged as pivotal biphasic regulators in the onset, progression, and resolution of ischemic stroke. This review synthesizes current evidence regarding the multifaceted roles of MMPs in stroke pathophysiology. Prior to ictus, MMPs increase vascular vulnerability by driving pathological remodeling in atherosclerosis and hypertension. During the acute phase, the rapid activation of MMP-2, -3, and - 9 degrades tight junction proteins (e.g., occludin, claudin-5, ZO-1) and extracellular matrix (ECM) components, precipitating blood-brain barrier (BBB) disruption, neuroinflammation, and hemorrhagic transformation. Conversely, during the subacute and recovery phases, MMP-2 and MMP-13 facilitate neurovascular unit (NVU) repair by promoting angiogenesis, synaptic plasticity, and ECM remodeling. Furthermore, we highlight the role of aberrant MMP signaling in mediating the brain-peripheral organ axis, which triggers sympathetic imbalance and systemic immune dysfunction. Despite promising preclinical results with small-molecule inhibitors and tissue inhibitors of metalloproteinases (TIMPs), clinical translation has been stifled by the nonspecific toxicity of broad-spectrum inhibitors and the inadvertent suppression of beneficial MMP functions during the repair phase. We conclude that the therapeutic paradigm must shift from broad-spectrum inhibition to precision regulation. Tailoring interventions to specific molecular subtypes, cell types, and temporal windows is essential. This review provides a theoretical framework for developing stage-specific MMP-targeted therapies to improve clinical outcomes in stroke patients. - Source: PubMed
Publication date: 2026/09/23
Wang PengWu Jia-WeiWang Bing-XinChen Cui-YanWu Chun-LinZhai Xiao-FuZhao Xu-Dong - Intervertebral disc degeneration (IDD) is driven by persistent inflammation, macrophage dysregulation, and ferroptosis-associated injury of nucleus pulposus cells (NPCs). Here, we developed an acid-responsive injectable hydrogel based on oxidized chondroitin sulfate and adipic acid dihydrazide-modified hyaluronic acid for sustained delivery of 5-aminosalicylic acid (5-ASA). Single-cell transcriptomic analysis and tissue validation revealed increased inflammatory macrophage infiltration and ferroptosis-associated alterations in degenerated discs. In vitro, 5-ASA preserved extracellular matrix homeostasis, reduced iron accumulation and MDA accumulation, and restored GPX4 expression in IL-1β-stimulated NPCs. It also suppressed LPS-induced M1-like macrophage polarization and promoted a reparative phenotype. Conditioned-medium and Transwell coculture experiments further showed that macrophage reprogramming contributed to the alleviation of ferroptosis-associated injury by 5-ASA in NPCs. NF-κB inhibition partially contributed to the protective effects of 5-ASA in NPCs and macrophages, while macrophage-conditioned medium was associated with altered NF-κB signaling in recipient NPCs. The resulting 5-ASA-loaded HACS hydrogel exhibited favorable injectability, porous architecture, acid-responsive degradation, sustained drug release, and good biocompatibility. In a rat IDD model, intradiscal administration of 5-ASA@HACS improved disc height and histological structure, preserved collagen II, reduced MMP13, suppressed p-p65, restored GPX4, and shifted macrophage polarization toward CD206-positive cells. These findings support 5-ASA@HACS as a biomaterial-based strategy for coordinated immunomodulatory and alleviation of ferroptosis-associated injury in IDD. - Source: PubMed
Publication date: 2026/09/18
Jiang YichenSun GuantongWei HaixinXiao HanwenXu DerongZhou Chuanli - Knee osteoarthritis (KOA) is a chronic degenerative joint disease characterized by cartilage destruction, subchondral bone remodeling, and inflammation. Gut microbiota dysbiosis and aberrant HDAC3/PPAR-γ signaling contribute to KOA progression. This study investigated the therapeutic effects of Renshenguben (RSGB) combined with swimming exercise in monosodium iodoacetate (MIA)-induced KOA and explored the underlying mechanisms. - Source: PubMed
Publication date: 2026/09/08
Huang ZiqiangHe ZhenhongYang MeiJiang XiaohuaZhang NingchuanBao Dingsu - This study aimed to establish and validate a rat model of patellofemoral osteoarthritis (PFOA) induced by patellar instability and to characterize its early degenerative features and compartment specificity. - Source: PubMed
Publication date: 2026/09/08
Yang FangliWang ZhenLi MengmengShi MingweiDiao JieyaoFan XuanqiangYang TaoZhou YunfengXu Hui