MMP1_RAT Mmp1 ELISA tesk kit
- Known as:
- MMP1_RAT Mmp1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen2553
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- EIAab
- Gene target:
- MMP1_RAT Mmp1 ELISA tesk kit
Ask about this productRelated genes to: MMP1_RAT Mmp1 ELISA tesk kit
- Gene:
- MMP1 NIH gene
- Name:
- matrix metallopeptidase 1
- Previous symbol:
- CLG
- Synonyms:
- -
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-02-23
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Qiu HeJi QiangChen CiqiongHuang JinWu Dongmei - -(), a traditional Chinese folk medicine, is recognized for its anti-inflammatory and analgesic properties. In this study, we report the extraction, purification, and anti-inflammatory mechanisms of C-glycosides from (ADCG). We developed an integrated strategy for the efficient enrichment and identification of polar C-glycosides from . Sample pretreatment via freeze-drying preserved thermolabile constituents, and reflux extraction with 60% aqueous ethanol optimized polar compound recovery. A key innovation was the implementation of a repeated-loading strategy using polyamide resin chromatography, which significantly enhanced the dynamic adsorption capacity and prevented leakage of target analytes. This approach achieved a 15.8-fold enrichment of target C-glycosides and enabled the identification of seven compounds, including chrysin- and apigenin-based derivatives. It effectively provides an efficient and cost-effective approach for the large-scale enrichment of this fraction. ADCG significantly suppressed granuloma formation in a cotton ball-induced model. In vitro, ADCG demonstrated potent anti-inflammatory effects in LPS-stimulated RAW264.7 macrophages by dose-dependently inhibiting the production of NO, TNF-α, and IL-6, without inducing cytotoxicity. In TNF-α-induced human rheumatoid arthritis synovial MH7A cells, ADCG inhibited proliferation, migration, invasion, and the secretion of pro-inflammatory mediators IL-6, IL-8, IL-1β, and MMP-1. Mechanistic investigations combining molecular docking and Western blot analysis revealed that ADCG directly inhibits NF-κB activation by suppressing IκBα degradation and p65 phosphorylation, thereby blocking nuclear translocation and the expression of downstream pro-inflammatory genes. Furthermore, constituents of ADCG exhibited high binding affinity for JAK2 and EGFR, suggesting a potential multitarget mechanism. These findings underscore the potential of ADCG as a complementary therapeutic agent for inflammatory diseases, particularly rheumatoid arthritis, and provide important insights into its molecular mechanisms of action. - Source: PubMed
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