Lunasin减轻大鼠运动性关节软骨损伤  

Lunasin alleviates the sports articular cartilage injury of rats

作　　者：刘粟[1,2] 邱勇[3] 刘红[3] 贾绍辉[4] 刘万红[1] LIU SU QIU Yong LIU Hong JIA Shao-hui LIU Wang-hong(School of Basic Medical Sciences, Wuhan University, Wuhan 430071 Science and Technology College of Hubei University for Nationalities, Enshi 445000 College of Medicine, Hubei University for Nationalities, Enshi 445000 College of Health Science, Wuhan Sports University, Wuhan 430079, China)

机构地区：[1]武汉大学基础医学院,湖北武汉430071 [2]湖北民族学院科技学院,湖北恩施445000 [3]湖北民族学院医学院,湖北恩施445000 [4]武汉体育学院健康学院,湖北武汉430079

出　　处：《基础医学与临床》2017年第5期691-695,共5页Basic and Clinical Medicine

基　　金：国家体育总局科研项目(2015B081)

摘　　要：目的探讨多肽Lunasin对运动性关节软骨损伤的治疗作用及机制。方法将大鼠随机分为对照组和模型组,在注射给予木瓜蛋白酶造模后,标准饲养28 d,然后将模型大鼠分为单纯模型组、0.01、0.05和0.1 mmol/L Lunasin治疗组(每组10只,治疗时间1个月)。治疗结束后分别用ELISA和RT-PCR检测血清及组织中IL-1β、IL-6、TNF-α、MMP-6及MMP-8 mRNA的表达;用试剂盒检测SOD活性及i NOS,用Western blot检测NRF2、Keap1、LC-3Ⅱ、Bax、Beclin1、p-AMPK和AMPK蛋白的表达。结果模型组中IL-1β、IL-6、TNF-α、MMP-6以及MMP-8在血清及组织中含量较对照组均显著升高(P<0.05),Lunasin治疗后上述因子均显著回降(P<0.05);并且Lunasin治疗能显著提高SOD的活性(P<0.05),上调NRF2的表达并降低i NOS的产生(P<0.05);另外,Lunasin能够上调受损关节软骨组织中自噬蛋白Beclin1以及LC-3Ⅱ的表达,抑制软骨细胞的凋亡蛋白Bax的表达。结论 Lunasin能够通过降低炎性介质的产生、激活氧化应激系统以及自噬通路,促进受损关节的修复。Objective To exploer the function and underlying mechanism of Lunasin on sports articular cartilage injury. Methods Wistar rats were randomly divided into 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. SOD activity and iNOS were evaluated by their ELISA kit. Western blot was used to detect the expression of NRF2, Keapl, LC-3 Ⅱ , Bax, Beclinl, p-AMPK, AMPK. Results Compared with control, the dose of IL-1 β, 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 increased SOD activity thase （iNOS） （P 〈 0.05 ） , up-regulated NRF2 expression and down-regulated the generation of nitric oxide syn Additionally, Lunasin can raise the expression of autophagy-related protein（beclin1 and LC-3 Ⅱ ） , reduce the expression of apoptosis protein （Bax） in damaged articular cartilage. Conclusions Lunasin benefits the repair of damaged joints by reducing the production of inflammatory mediators, activating of oxidative stress system and autophagy pathway.

关 键 词：Lunasin 凋亡 自噬 运动性关节软骨损伤 

分 类 号：R684.7[医药卫生—骨科学]