| Objective To explore the protective effect of astragalus glycosides on knee osteoarthritis (KOA) rats and it impact on JNK/p38MAPK signaling pathway. Methods Ninety SD rats were separated into sham operation group, model group, celecoxib group (18 mg/kg), astragalus low (25 mg/kg), medium (50 mg/kg), high (100 mg/kg) dose groups randomly, 15 per group. The modified Huith method was performed to establish the KOA model, Postoperative gavage lasted for 6 weeks. The diameter of the rat’s knee joint was measured with a vernier caliper, and the toe volume of the rat was measured with a toe volume meter; serum LEVELS of IL-1β, IL-6 and TNF-α were determined by ELISA; HE staining was used to observe the pathological changes of knee cartilage. The contents of TGF-β1 and MMP-3 in cartilage tissue were detected by ELISA. The protein expressions of P-JNK, JNK, P-P38MAPK and p38MAPK were detected by Western Blot. Results Compared with the sham operation group, the surface of the cartilage tissue in the model group was destroyed, the tissue layer became thinner, the number of cells was reduced and the arrangement was disordered, and the tide line was largely destroyed; the diameter of the knee joint and the volume of the toes increased obviously (P<0.05); the serum IL-1β, IL-6, TNF-α contents and cartilage tissue TGF-β1, MMP-3 contents, p-JNK/JNK, p-38MAPK/ p38MAPK ratio increased obviously (P<0.05). Compared with the model group, the cartilage tissue lesions of the celecoxib group and the astragalus glycoside groups were obviously reduced; the diameter of the knee joint and the volume of the toes reduced obviously (P<0.05); the serum IL-1β, IL-6, TNF-α contents and cartilage tissue TGF-β1, MMP-3 contents, p-JNK/JNK, p-38MAPK/p38MAPK ratio reduced obviously (P<0.05), and there was a dose effect among the different dose Astragalus glycosides groups (P<0.05); There was no significant difference in the above indicators between the high-dose Astragalus glycoside group and the celecoxib group (P>0.05). Conclusion: Astragalus glycosides may inhibit the activation of the JNK/p38MAPK signaling pathway, reduce inflammation, and improve the cartilage damage of the knee joint in KOA rats. |