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Updated: Apr 10, 2026
Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
Ginsenoside Rb1 inhibits matrix metalloproteinase 13 through down-regulating Notch signaling pathway in
Wei Wang1, Li Zeng2, Ze-ming Wang2
1Department of Combination of Chinese and Western Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China Department of Traditional Chinese Medicine for Tumor, Chongqing Cancer Institute, Chongqing 400030, PR China.
Abstract:
Mounting evidence suggests that an excess of matrix metalloproteinase-13 (MMP-13) plays an important role in the breakdown of extracellular matrix in osteoarthritis (OA). Here, the effects of ginsenoside Rb1 (GRb1) on the expression of MMP-13 in IL-1β-induced SW 1353 chondrosarcoma cells and an experimental rat model of OA induced by anterior cruciate ligament transection (ACLT) were investigated. SW1353 chondrosarcoma cells were pretreated with or without GRb1 and Notch signaling pathway inhibitor, DAPT, then were stimulated with IL-1β. In rats, experimental OA was induced by ACLT. These rats then received intra-articular injections of vehicle, an inhibitor of γ-secretase, DAPT, and/or GRb1. Expression of MMP-13, collagen type II (CII), Notch1, and jagged 1 (JAG1) were verified by western blotting and immunohistochemistry. In addition, levels of MMP-13 mRNA were detected using quantitative real-time PCR. In histological analyses, treatment with DAPT reduced the number of cartilage lesions present and the expressions of MMP-13, CII, Notch1, and JAG1. In addition, treatment with GRb1 was associated with lower levels of Notch1 and JAG1 in both IL-1β-induced SW1353 chondrosarcoma cells and in the rat OA model. Furthermore, the suppressive effect of GRb1 on MMP-13 was greater than that exhibited by the signaling pathway inhibitor. In conclusion, GRb1 inhibits MMP-13 through down-regulating Notch signaling pathway in OA.
Insights
Ginsenoside Rb1 (GRb1) may treat osteoarthritis by reducing matrix metalloproteinase-13 (MMP-13) via the Notch signaling pathway. This natural compound shows promise in both cell and animal models of osteoarthritis.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Osteoarthritis (OA) involves extracellular matrix breakdown, often linked to excess matrix metalloproteinase-13 (MMP-13).
- Ginsenoside Rb1 (GRb1) is a compound with potential therapeutic properties.
Purpose of the Study:
- To investigate the effects of GRb1 on MMP-13 expression in osteoarthritis.
- To explore the role of the Notch signaling pathway in GRb1's mechanism of action.
Main Methods:
- Utilized IL-1β-induced SW1353 chondrosarcoma cells and an anterior cruciate ligament transection (ACLT) rat model for osteoarthritis.
- Assessed MMP-13, collagen type II (CII), Notch1, and jagged 1 (JAG1) expression via western blotting, immunohistochemistry, and quantitative real-time PCR.
- Administered GRb1 and DAPT (Notch signaling inhibitor) in cellular and animal models.
Main Results:
- DAPT treatment reduced cartilage lesions and expression of MMP-13, CII, Notch1, and JAG1.
- GRb1 treatment lowered Notch1 and JAG1 levels in both cell and OA rat models.
- GRb1 demonstrated a stronger suppressive effect on MMP-13 than DAPT.
Conclusions:
- Ginsenoside Rb1 inhibits MMP-13 expression in osteoarthritis.
- GRb1 exerts its effects by down-regulating the Notch signaling pathway.
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