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.