ReferenceID 6130
Quercitrin alleviates cartilage extracellular matrix degradation and delays ACLT rat osteoarthritis development: An in vivo and in vitro study
J Adv Res
Introduction: Disruptions of extracellular matrix (ECM) degradation homeostasis play a significant role in the pathogenesis of osteoarthritis (OA). Matrix metalloproteinase 13 (MMP13) and collagen II are important compon
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- Reference Id
- 6130
- Evidence Id
- 22720
- Core Evidence Id
- 22720
- Source Reference Id
- 5524
- Herb2 Reference Id
- HBREF006321
- Subject Paper Key
- HBIN041726_33364061
- Pubmed Id
- 33364061
- Doi
- 10.1016/j.jare.2020.06.020
- Paper Title
- Quercitrin alleviates cartilage extracellular matrix degradation and delays ACLT rat osteoarthritis development: An in vivo and in vitro study
- Paper Abstract
- Introduction: Disruptions of extracellular matrix (ECM) degradation homeostasis play a significant role in the pathogenesis of osteoarthritis (OA). Matrix metalloproteinase 13 (MMP13) and collagen II are important components of ECM. Earlier we found that quercitrin could significantly decrease MMP13 gene expression and increase collagen II gene expression in IL-1beta-induced rat chondrocytes and human chondrosarcoma (SW1353) cells. Objectives: The effects and mechanism of quercitrin on OA were explored. Methods: Molecular mechanisms of quercitrin on OA were studied in vitro in primary chondrocytes and SW1353 cells. An anterior cruciate ligament transection (ACLT) rat model of OA was used to investigate the effect of quercitrin in vivo. Micro-CT analysis and Safranin O-Fast Green Staining of knee joint samples were performed to observe the damage degree of tibial subchondral bone. Immunohistochemistry of knee joint samples were conducted to observe the protein level of MMP13, collagen II and p110alpha in articular cartilage. Results: In vitro, quercitrin promoted cell proliferation and delayed ECM degradation by regulating MMP13 and collagen II gene and protein expressions. Moreover, quercitrin activated the Phosphatidylinositol 3-kinase p110alpha (p110alpha)/AKT/mTOR signaling pathway by targeting p110alpha. We also firstly showed that the gene expression level of p110alpha was remarkably decreased in cartilage of OA patients. The results showed that intra-articular injection of quercitrin increased bone volume/tissue volume of tibial subchondral bone and cartilage thickness and reduced the Osteoarthritis Research Society International scores in OA rats. Meanwhile, immunohistochemical results showed that quercitrin exerted anti-OA effect by delaying ECM degradation. Conclusion: These findings suggested that quercitrin may be a prospective disease-modifying OA drug for prevention and treatment of early stage OA.
- Journal
- J Adv Res
- Publish Year
- 2020
- Experiment Subject
- rat; human; patient; human chondrosarcoma (sw1353) cells; il-1beta-induced rat chondrocytes; sw1353 cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Osteoarthritis; Anterior Cruciate Ligament Transection; Chondrosarcoma
- Paper Title Cn
- Paper Title En
- Quercitrin alleviates cartilage extracellular matrix degradation and delays ACLT rat osteoarthritis development: An in vivo and in vitro study
- Bilingual Status
- semi_complete