Abstract
BACKGROUND: Osteoarthritis (OA) of the knee joint is a prevalent joint disease that affects most aging individuals worldwide. An extract of garlic oil, diallyl disulfide (DADS), reportedly protects chondrocytes in vitro, with limited data available on its in vivo OA effects. We explored the efficacy of DADS in ovariectomy (OVX)-induced OA rats. METHODS: In this study, thirty-four female Sprague-Dawley rats were used. Twenty-three rats underwent a bilateral OVX and the remaining rats underwent a sham procedure. Six weeks post-surgery, five OVX rats and five SHAM rats were sacrificed. The histological methods and micro-CT were used to assess the success of the OVX-OA model. Meanwhile, six OVX rats were administered 100ul hydrogel and these rats were defined as the OVX + Vehicle group. Six OVX rats received 100ul hydrogel with 50 mg/mL DADS once, while another six OVX rats received 100ul hydrogel with 500 mg/mL DADS once, both by a single knee joint injection. The remaining SHAM rats received a single knee joint injection of equivalent saline. Four weeks post-administration, the bone mineral density (BMD) and subchondral trabecular microstructure were measured. Cartilage erosion was assessed by histological observation, while type II collagen (CII), matrix metalloproteinase (MMP)-13 in articular cartilage, and osteopontin (OPN) in subchondral bone by immunohistochemistry. RESULTS: At six weeks after OVX, there was significant cartilage erosion and more bone loss in the OVX rats than the sham rats. At ten weeks post-surgery, DADS hydrogel significantly increased BMD and suppressed subchondral bone trabecular loss caused by OVX. Furthermore, DADS significantly rescued cartilage erosion and improved cartilage metabolism by decreasing MMP-13 and increasing CII expressions. Moreover, OPN expression increased in the OVX + Vehicle group than SHAM group; DADS inhibited this increase. CONCLUSION: These results suggest that DADS retards early OA progression in an OVX-OA rat model by improving cartilage metabolism and preventing the deterioration of subchondral bone microstructure, presenting a potential agent for ameliorating postmenopausal OA progression.