食品科学 ›› 2019, Vol. 40 ›› Issue (5): 143-148.doi: 10.7506/spkx1002-6630-20171114-166

• 营养卫生 • 上一篇    下一篇

乙酯型鱼油对小鼠骨性关节炎的改善作用

王 凯,朱玉婕,李媛媛,戴宇峰,王玉明,王静凤*   

  1. 中国海洋大学食品科学与工程学院,山东 青岛 266003
  • 出版日期:2019-03-15 发布日期:2019-04-02
  • 基金资助:
    “十三五”国家重点研发计划项目(2017YFF0207805);山东省重点研发计划项目(2016YYSP017)

Ethyl Ester Type Fish Oil Attenuates Posttraumatic Osteoarthritis in Mice

WANG Kai, ZHU Yujie, LI Yuanyuan, DAI Yufeng, WANG Yuming, WANG Jingfeng*   

  1. College of Food Science and Engineering, Ocean University of China, Qingdao 266003, China
  • Online:2019-03-15 Published:2019-04-02

摘要: 目的:研究乙酯型鱼油(fish oil,FO)对骨性关节炎小鼠软骨退变的改善作用。方法:9 周龄雄性C57BL/6J小鼠构建内侧半月板不稳骨性关节炎模型。术后8 周,随机分成假手术组、模型对照组、阳性对照组和FO低、高剂量组。每天灌胃1 次,持续灌胃60 d后,取关节软骨组织行苏木精-伊红染色、甲苯胺蓝染色及实时荧光定量聚合酶链式反应(quantitative real-time polymerase chain reaction,qPCR)分析。结果:苏木精-伊红和甲苯胺蓝染色分析表明FO能够显著改善软骨结构,维持软骨基质的稳定。qPCR结果表明,FO能显著提高Acan、Col2α1的mRNA表达,维持软骨细胞正常表型;抑制Col10α1、Runx-2、Bcl-2、Bax和Caspase-3的表达,抑制软骨细胞的肥大分化及异常凋亡。同时,FO能够显著降低mTOR的mRNA表达,提高LC-3B和ATG-5的mRNA表达,促进自噬进程,维持软骨的稳态。结论:FO能够通过激活软骨细胞自噬进程来抑制骨性关节炎小鼠的软骨退变进程。

关键词: 乙酯型鱼油, 骨性关节炎, 软骨退变, 成熟肥大, 凋亡, 自噬

Abstract: Objective: To investigate the improving effect of ethyl ester type fish oil (FO) on cartilage degeneration in mice with posttraumatic osteoarthritis. Methods: Nine-week-old male C57BL/6J mice were used to establish an animal model of osteoporosis induced by surgical destabilization of the medial meniscus (DMM). At 7 weeks after the operation, these mice were randomly divided into four groups: sham control group, osteoporosis model, positive control, low-dose FO, and high-dose FO groups. All the animals were orally administered once daily for 60 days. After the administration period, cartilage was harvested for HE staining, toluidine blue staining and quantitative real-time polymerase chain reaction (qPCR) analysis. Results: HE and toluidine blue staining indicated that FO could significantly improve the structure of cartilage and maintain its homeostasis. qPCR results revealed that FO remarkably increased the mRNA expression of Acan and Col2α1, thereby maintaining normal chondrogenic phenotype. Meanwhile, FO significantly decreased the mRNA expression of Col10α1, Runx2, Bcl-2, Bax and caspase-3, thus inhibiting chondrocyte hypertrophy and apoptosis. Mechanistically, FO could activate autophagy through up-regulating the mRNA expression of autophagy-related genes such as LC-3B and ATG5 and suppressing the mRNA expression of mTOR. Conclusion: FO can inhibit cartilage degeneration through activating chondrocyte autophagy in mice with osteoarthritis.

Key words: ethyl ester type fish oil, osteoarthritis, cartilage degeneration, hypertrophy, apoptosis, autophagy

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