Abstract: BACKGROUND: Ginseng extracts have been found to significantly improve osteoarthritis, but the therapeutic effects of ginseng polysaccharide extracts on osteoarthritis have not been reported.
OBJECTIVE: To investigate the effect of ginseng polysaccharide on the expression of prostaglandin E2/6-keto-prostaglandin F1α in traumatic osteoarthritis model rats.
METHODS: Sixty male Sprague-Dawley rats were selected and randomly divided into healthy group, model group, ginseng polysaccharide low-dose group, ginseng polysaccharide medium-dose group, ginseng polysaccharide high-dose group and dexamethasone group. Except for 10 rats in the healthy group, the other rats were taken to establish traumatic osteoarthritis models. The healthy group and model group were given 0.2 mL of normal saline intraperitoneally. The low-, medium-, and high-dose groups were intraperitoneally injected with 0.1, 0.25, 0.5 μg/mL ginseng polysaccharide, respectively. In the dexamethasone group, 0.2mg/kg dexamethasone (0.2 mL) was injected intraperitoneally. Injections were given once every 3 days, for 4 consecutive weeks. Serum prostaglandin E2 and 6-keto-prostaglandin F1α levels were detected by ELISA. The bone and joint function of rats were assessed by the Mankin’s score. Hematoxylin-eosin staining was used to observe the pathologic morphology of the knee joints of rats. Western blot and PCR were used to detect the protein and mRNA expression of tumor necrosis factor α and interleukin-1β, interleukin-10 in articular cartilage tissue, respectively.
RESULTS AND CONCLUSION: Compared with the model group, serum prostaglandin E2 levels were decreased in the medium-dose group and dexamethasone group, while serum 6-keto-prostaglandin F1α levels were increased (P < 0.05). Compared with the medium-dose group and dexamethasone group, the above-mentioned indicators were significantly improved in the high-dose group, and there was no significant difference between the medium-dose group and dexamethasone group (P > 0.05). Compared with the model group, the Mankin’s score was reduced in the medium-dose group and dexamethasone group (P < 0.05), but there was no significant difference between the medium-dose group and dexamethasone group (P > 0.05). Compared with the medium-dose group and dexamethasone group, the Mankin’s score was significantly reduced in the high-dose group (P < 0.05). The cartilage tissue layer of rats in the model and low-dose groups was significantly thinned, the cracks and chondrocytes deep into the bone layer were largely lost, the tide line was seriously broken and blurred, the collagen fibers in the synovial layer were increased and thickened, and a large number of chondrocytes were destroyed and arranged irregularly. These pathological changes were improved in the medium-dose group and dexamethasone group compared with the model group as well as improved in the high-dose group compared with the medium-dose group. Compared with the model group, the expression of tumor necrosis factor-α and interleukin-1β was reduced, while the expression of interleukin-10 was increased in the medium-dose group and dexamethasone group (P < 0.05). These indicators in the joint were significantly improved in the high-dose group compared with the medium-dose group and dexamethasone group (P < 0.05), but there was no significant difference between the medium-dose group and dexamethasone group (P > 0.05). To conclude, ginseng polysaccharide can improve the inflammatory level and pathological morphology of traumatic osteoarthritis rats and reduce the Mankin’s score. Its mechanism may be related to the regulation of prostaglandin E2/6-keto-prostaglandin F1α levels.

Key words: ginseng polysaccharide, traumatic osteoarthritis, prostaglandin E2, 6-keto-prostaglandin F1α, animal model