Journal of orthopaedic translation · 2016
Translational potential of ginsenoside Rb1 in managing progression of osteoarthritis.
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Chen Yuanfeng, Lin Sien, Sun Yuxin, Pan Xiaohua, Xiao Liubin, Zou Liyi, Ho Ki Wai, Li Gang
Аннотация
BACKGROUND: Osteoarthritis (OA) is the most common degenerative joint disorder. Inflammatory cytokine plays an important role in OA progression. Previous studies have demonstrated that ginsenoside Rb1 would prevent inflammation and apoptosis in chondrocytes. However, we have not found any animal study reporting that Rb1 attenuates the severity of OA.
OBJECTIVE: In this study, we used a rat anterior cruciate ligament transaction plus medial meniscus resection (ACLT + MMx) model of OA and a cell model, to investigate whether administration of ginsenoside Rb1 may attenuate the progression of arthritis.
METHODS: In this in vivo study, 16-week-old male Sprague-Dawley rats were divided into three groups: Group 1 (sham control group), Group 2 (Rb1-treated group), and Group 3 (OA group). In Groups 2 and 3, OA was induced in the right knee joint with ACLT + MMx in rats. Then Group 2 received continuous infusion of ginsenoside Rb1 via osmotic mini-pumps implanted subcutaneously. At 4 weeks after treatment, the rats were sacrificed. Interleukin-1β (IL-1β) level was evaluated by enzyme-linked immunosorbent assay (ELISA); cartilage damage was assessed via histology (Safranin-O/fast green stain) and immunohistochemistry [matrix metalloproteinase-13 (MMP13) and type X collagen (Col X)]. For cell study, C5.18 (rat chondrocyte cell line) was used in this research. The effect of Rb1 on IL-1β-induced MMP13 or Col X expression level in C5.18 cells was investigated.
RESULTS: In this in vivo study, characteristics of OA were present in the OA group, in contrast to less severe damage generally observed in the Rb1 treatment group: first, IL-1β level was significantly decreased, and second, cartilage degeneration was attenuated, as indicated by lower histologic damage scores and lower percentages of MMP13 or Col X-positive chondrocytes. In the cell study, the results showed that Rb1 treatment would relieve the MMP13 or Col X expression in C5.18 cells induced by IL-1β.
CONCLUSION: In the present study, we demonstrated that Rb1 can attenuate the progression or severity of arthritis by reducing inflammation.
OBJECTIVE: In this study, we used a rat anterior cruciate ligament transaction plus medial meniscus resection (ACLT + MMx) model of OA and a cell model, to investigate whether administration of ginsenoside Rb1 may attenuate the progression of arthritis.
METHODS: In this in vivo study, 16-week-old male Sprague-Dawley rats were divided into three groups: Group 1 (sham control group), Group 2 (Rb1-treated group), and Group 3 (OA group). In Groups 2 and 3, OA was induced in the right knee joint with ACLT + MMx in rats. Then Group 2 received continuous infusion of ginsenoside Rb1 via osmotic mini-pumps implanted subcutaneously. At 4 weeks after treatment, the rats were sacrificed. Interleukin-1β (IL-1β) level was evaluated by enzyme-linked immunosorbent assay (ELISA); cartilage damage was assessed via histology (Safranin-O/fast green stain) and immunohistochemistry [matrix metalloproteinase-13 (MMP13) and type X collagen (Col X)]. For cell study, C5.18 (rat chondrocyte cell line) was used in this research. The effect of Rb1 on IL-1β-induced MMP13 or Col X expression level in C5.18 cells was investigated.
RESULTS: In this in vivo study, characteristics of OA were present in the OA group, in contrast to less severe damage generally observed in the Rb1 treatment group: first, IL-1β level was significantly decreased, and second, cartilage degeneration was attenuated, as indicated by lower histologic damage scores and lower percentages of MMP13 or Col X-positive chondrocytes. In the cell study, the results showed that Rb1 treatment would relieve the MMP13 or Col X expression in C5.18 cells induced by IL-1β.
CONCLUSION: In the present study, we demonstrated that Rb1 can attenuate the progression or severity of arthritis by reducing inflammation.