Eucommia ulmoides Oliv. bark aqueous extract inhibits osteoarthritis in a rat model of osteoarthritis

Eucommia ulmoides Oliv. bark (EU) is a common traditional Chinese herbal medicine for treatment of osteoarthritis (OA), but its therapeutic effect on OA and the underlying mechanisms have not been fully clarified. Our previous study showed that Eucommia ulmoides Oliv. bark aqueous extract (EUE) had a protective effect on cartilage, and this study was aimed to investigate the anti-osteoarthritis effect and mechanisms of EUE in a rat model of osteoarthritis. Thirty-two 5-week-old specific pathogen-free Sprague–Dawley rats which were randomized into four even groups (n=8). Group A received sham operation while the OA model was established using the modified Hulth technique in groups B, C and D. For eight weeks after operation, in addition to routine feeding, group A received gavage with deionized water, group B with deionized water, group C with 1.35 g/kg/day EUE, and group D with 2.7 g/kg/day EUE. Eight weeks postoperatively, all of the animals were euthanized for radiological, gross and histopathological observations to evaluate the effect of EUE on OA and to determine its potential mechanisms. Radiological and histopathological observations showed that the articular degenerative changes were significantly more alleviated in groups C and D than in group B, while there were no obviously degenerative manifestations in group A. Mankin׳s scores in groups C and D were significantly lower than in group B (P<0.01). The severity of OA was significantly less in group D than in group C (P<0.01). The IL-1β and IL-6 contents in serum and MMP-3 secretion in articular cartilage were significantly lower in groups C and D than those in group B (P<0.01), and significantly lower in group D than those in group C (P<0.01). Compared with group B, phosphorylated Akt was significantly down-regulated in groups C and D. EUE may inhibit the progression of osteoarthritis by inhibiting the PI3K/Akt pathway to delay cartilage degeneration, reduce inflammatory cytokines and prevent MMP-3 secretion. Therefore, EU is a potential therapeutic agent for OA, but its efficacy is limited.