MMP9 Antibody
- Known as:
- MMP9 Antibody
- Catalog number:
- 29091
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- MMP9 Antibody
Related genes to: MMP9 Antibody
- Gene:
- MMP9 NIH gene
- Name:
- matrix metallopeptidase 9
- Previous symbol:
- CLG4B
- Synonyms:
- -
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-14
- Date modifiied:
- 2015-02-23
Related products to: MMP9 Antibody
Related articles to: MMP9 Antibody
- Osteoarthritis (OA) is a chronic degenerative joint disease characterized by progressive cartilage destruction and persistent low-grade inflammation, in which extracellular matrix (ECM) homeostasis plays a pivotal role. Although oyster hydrolysate (OH), derived from (), is rich in bioactive peptides and has antioxidant and anti-inflammatory properties, its effects on the pathogenesis of OA have not yet been studied. This study aimed to investigate the anti-inflammatory and chondroprotective effects of OH using and OA models. - Source: PubMed
Publication date: 2026/03/19
Ji Seon YeongHwangbo HyunKim Min YeongKim Da HyeHong Su HyunShim Jung-HyunMoon Sung-KwonKim Gi-YoungCho SuengmokChoi Yung Hyun - Diabetes mellitus and periodontitis share a bidirectional inflammatory relationship. Oral fluids provide non-invasive access to host and microbial signals relevant to both diseases, but clinical translation of oral fluid biomarkers in diabetic periodontitis remains limited. - Source: PubMed
Publication date: 2026/07/28
Toby Thomas JulieJoseph BetsyAji Nur R A SThomas TobySorsa TimoAnil SukumaranWaltimo Tuomas - This study aimed to evaluate the potential of Acer truncatum leaf extract (ATLE) to mitigate oxidative-stress-induced impairment of reproductive function in laying hens, with a focus on mechanisms involving antioxidant defense, angiogenesis, and ovarian microenvironment homeostasis. Oxidative stress was induced by tert-butyl hydroperoxide (tBHP) injection. Hens were randomly assigned to a control group (CON), an oxidative stress group (BCON), and an oxidative stress group supplemented with 0.6% ATLE (BATLE). Egg-laying performance, ovarian morphology, reproductive hormones, oxidative stress markers, and angiogenesis indicators were evaluated and integrated with transcriptomic analysis. The results were as follows: 1) Production and Morphology: ATLE supplementation alleviated (P < 0.05) the tBHP-induced decrease in egg laying rate and elevation in feed conversion ratio (FCR). It also mitigated (P < 0.05) reductions in the number of hierarchical follicles and the ovarian stroma index while restoring (P < 0.05) serum concentrations of LH and GH, thereby re-establishing reproductive endocrine balance. 2) Antioxidant Defense: ATLE activated (P < 0.05) Nrf2 and increased (P < 0.05) transcription of downstream antioxidant genes, including SOD3, GPX3, PRDX4, GSR and CAT, thereby enhancing (P < 0.05) the SOD and CAT activities and reducing (P < 0.05) MDA concentrations within both serum and ovarian tissues. 3) Vascular Network Support: ATLE attenuated (P < 0.05) the tBHP-induced downregulation of angiogenic factors, including protein levels of VEGF, ANGPT1, and HIF-1α and mRNA expression levels of VEGFA, ANGPT1, ANGPT2, ITGA5, and MMP9. 4) Microenvironment Remodeling: Transcriptomic integration revealed that ATLE-mediated repair overlapped (> 88%) with oxidative-stress-induced damage across functional modules. By reversing dysregulation of key genes such as VEGFA, KDR, and FN1, ATLE restored core pathways including focal adhesion and ECM-receptor interaction, and coordinated processes such as extracellular matrix, angiogenesis, and response to wounding, driving a systemic remodeling of the ovarian reproductive microenvironment toward homeostasis. In summary, this study demonstrated that ATLE activated multiple signaling axes, notably Nrf2 and VEGF. As a result, ATLE enhanced antioxidant defenses against oxidative damage and promoted vascular health and microenvironmental remodeling in the ovary. Together, these effects preserved the structural integrity and function of the laying hen reproductive system. These findings supported the potential of ATLE as a natural feed additive and provided a scientific rationale for using nutritional strategies to alleviate oxidative stress and improve reproductive health in laying hens. - Source: PubMed
Publication date: 2026/08/12
Qin KailongMa JunjieGao MingluLiu YanliYang Xiaojun - Breast cancer remains a major cause of morbidity and mortality in women, with around 2.3 million new cases and 670,000 deaths worldwide in 2022. Daidzin, a soy isoflavone glycoside from Glycine max, is a candidate bioactive scaffold, but its breast cancer-relevant mechanisms remain poorly defined. This study used an integrated in silico strategy combining network pharmacology and molecular modeling to prioritize daidzin targets and validate key interactions, with sirtinol as a reference compound. Target prediction identified 101 putative daidzin targets, and intersection with breast cancer-associated genes yielded 97 common targets. Protein-protein interaction analysis highlighted hub genes including ALB, TNF, MMP9, CASP3, SRC, ITGB1, MMP2, ESR1, IL2, and HSP90AA1. Enrichment analyses suggested convergence on extracellular/vesicle-related functions, metallopeptidase activity, and pathway modules spanning metabolism, inflammation, endocrine signaling, and cancer circuitry. Docking against ten hub proteins produced binding energies from -6.00 to -11.49 kcal/mol, with the strongest affinity for MMP9 (6ESM; -11.49 kcal/mol), exceeding B9Z (-10.54 kcal/mol) and sirtinol (-10.59 kcal/mol). Molecular dynamics simulations indicated stable complexes, and Molecular Mechanics Generalized Born Surface Area (MMGBSA) supported stronger binding for daidzin-MMP9 (-46.86 ± 3.83 kcal/mol) than sirtinol-MMP9 (-14.12 ± 8.99 kcal/mol). Absorption, Distribution, Metabolism, Excretion, and Toxicity (ADMET) prediction indicated favorable safety-related flags for daidzin, although lower predicted intestinal absorption and Caco2 permeability than sirtinol suggest potential exposure-related limitations. Density Functional Theory (DFT) analysis supported comparatively greater electronic stability. Collectively, the results prioritize a daidzin-MMP9 axis for experimental validation. - Source: PubMed
Publication date: 2026/08/11
Vu Lan ThiVu Luong TrongVu Lien Thi KimPho Hang Thi ThuyNguyen Quan HuuNguyen Lan Thi NgocNguyen Yen Thi HaiNguyen Hung DucChu Mau Hoang - Acute kidney injury (AKI) is a severe clinical syndrome, with ischemia/reperfusion (I/R) being one of its most common causes. Although D‑pinitol (DP), an inositol‑like bioactive molecule, is known to confer renal protection, its efficacy against I/R‑induced AKI remains unknown. A mouse kidney I/R model was employed to evaluate the renoprotective effect of DP. Relevant targets associated with DP and AKI were retrieved from publicly available databases. Subsequently, network pharmacology analysis was conducted to identify the potential targets and signaling pathways. Molecular docking was then performed to predict the binding affinity of DP to core targets identified. Furthermore, and experiments were performed to validate these findings. Systemic toxicity was assessed by serological and histopathological examinations. The results show that DP significantly attenuated I/Rinduced kidney dysfunction and apoptosis. Network pharmacology analysis identified 108 overlapping targets, with AKT1, HSP90AA1, SRC, CASP3, and MMP9 identified as core targets. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed PI3K/AKT signaling pathway as the primary mechanism. Consistent with these predictions, DP enhanced PI3K and AKT phosphorylation in kidney tissue. Molecular docking indicated that DP exhibited the strongest binding affinity to SRC, suggesting it as a potential target. In a hypoxia/reoxygenation (H/R)-induced human renal proximal tubular epithelial (HK-2) cell model, DP significantly increased the phosphorylation of SRC, PI3K, and AKT, and these effects were abrogated by the SRC specific inhibitor PP2. Collectively, DP alleviated I/R‑induced injury and apoptosis, potentially through activation of the SRC/PI3K/AKT signaling pathway. - Source: PubMed
Publication date: 2026/08/10
Ren YilinGe YuanZhang KeyuLin HuiNiu DanHan WeixiaSu XiaoleWang LihuaQiao Xi