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- 2016
绿原酸对高强度运动引起的膝关节软骨损伤的保护作用
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Abstract:
摘要：目的 探讨绿原酸在高强度运动引起的大鼠膝关节软骨损伤中的保护作用及其可能的机制。方法 将同龄SD大鼠随机分为3组：运动组、干预组和对照组。运动组和干预组大鼠每天在自制电刺激运动装置中进行一次持续40min的跳跃运动，中间休息10min，每周运动6d，休息1d；干预组在每日运动前，给予腹腔注射绿原酸；对照组无任何处理。4周后，取含左后肢膝关节液的生理盐水用ELISA法测定其中白介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)、基质金属蛋白酶-3(MMP-3)含量和MMP-3酶活性，并利用蕃红染色评估膝关节软骨损伤情况。结果 与对照组相比，运动组大鼠膝关节软骨表面不光滑，出现很多微小裂隙，滑膜肿胀，软骨细胞增多紊乱，基质中糖胺多糖含量减少，关节液中IL-1β、TNF-α含量明显升高，MMP-3含量和酶活性均升高；而干预组大鼠膝关节软骨损伤程度较运动组轻，关节液中IL-1β、TNF-α含量、MMP-3含量和酶活性均低于运动组。结论 绿原酸对高强度跳跃运动引发的膝关节软骨损伤具有一定的保护作用，抑制炎症因子介导的MMP-3活化可能是其发挥上述保护作用的主要机制之一。
ABSTRACT: Objective To study the protective effects and mechanism of chlorogenic acid on articular cartilage injury induced by high-intensity exercises. Methods SD rats were randomly divided into 3 groups: exercise group, treatment group and control group. The rats of both exercise and treatment groups were trained in an autonomous exercise equipment with electric stimulation, 40min/d for 4 weeks, with 10min/time and 1d/w rest. At the same time, chlorogenic acid was intraperitoneally injected into the rats of exercise group once a day and no treatment was given to rats of the control group. After 4 weeks, the synovial fluid of knee joint was extracted and the levels of IL-1β, TNF-α, matrix metalloproteinase-3 (MMP-3) and its activity were examined by ELISA. At the same time, knee joint injury was evaluated with Sweet red dye. Results Compared with those in the rats of the control group, some tiny cranny and swollen synovia were shown in the cartilage of knee joint, along with an increasing number of disordered chondrocytes and less glycosaminoglycan in the rats of the exercise group. Besides, the levels of IL-1β, TNF-α, MMP-3 and its activity were all increased. However, the cartilage injury was alleviated in the treatment group, accompanied with relative lower levels of IL-1β, TNF-α, MMP-3 and its activity than those in the exercise group. Conclusion Chlorogenic acid could protect the articular cartilage against the injury induced by high-intensity exercises by suppressing inflammatory factor-induced MMP-3 activation
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