关键词: Lunasin, 凋亡, 自噬, 运动性关节软骨损伤

Abstract: Objective To exploer the function and underlying mechanism of Lunasin on sports articular cartilage injury. Methods Wistar rats were randomly divided into negative control group and model group; after injection molding for 3 times, the model rats were feed for 28 days. Then the model rats were divided into sham model group, 0.01, 0.05 and 0.1 mmol/L Lunasin treatment group respectively. After treatment, ELISA was used to analyze the production of IL-1β、IL-6、TNF-α、MMP-6 and MMP-8. The SOD activity and iNOS were evaluated by their ELISA kit. Western blot was used to detect the expression of NRF2, Keap1, LC-3Ⅱ, Bax, Beclin1, p-AMPK, AMPK. Results Compared with control, the dose of IL-1β、IL-6、TNF-α、MMP-6 and MMP-8 in serum of model rats were significantly increased (P < 0.05), however, after treatment with lunasin for 1 month, these inflammatory factors were obviously reduced then that of model rats (P < 0.05); Furthermore Lunasin treatment obviously increase SOD activity、up-regulate NRF2 expression and down-regulate the generation of nitric oxide synthase (iNOS) (P < 0.05); Additionally, Lunasin can raise the expression of autophagy-related protein(beclin1 and LC-3Ⅱ), reduce the expression of apoptosis protein (Bax) in damaged articular cartilage. Conclusion Lunasin benefit the repair of damaged joints by reducing the production of inflammatory mediators, activating of oxidative stress system and autophagy pathway.

Key words: Luansin, apoptosis, autophagy, sports articular cartilage injury