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山东大学学报(医学版) ›› 2016, Vol. 54 ›› Issue (9): 41-47.doi: 10.6040/j.issn.1671-7554.0.2015.898

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在慢性睡眠剥夺中骨桥蛋白通过NF-kappaB通路对颞下颌关节的影响

丁凤1,董亚兵2,赵华强2,朱国雄3,吴高义3   

  1. 1.锦州医科大学实习基地济南军区总医院口腔科, 山东 济南 250031;2.山东大学口腔医学院 山东省口腔组织再生重点实验室, 山东 济南 250012;3.中国人民解放军济南军区总医院口腔科, 山东 济南 250031
  • 收稿日期:2015-09-22 出版日期:2016-09-10 发布日期:2016-09-10
  • 通讯作者: 吴高义. E-mail:fmmugaoyi@163.com E-mail:fmmugaoyi@163.com
  • 基金资助:
    国家自然科学基金(81400573)

Effect of osteopontin through NF-kappaB signaling pathway in the temporomandibular joint of rats subjected to chronic sleep deprivation

DING Feng1, DONG Yabing2, ZHAO Huaqiang2, ZHU Guoxiong3, WU Gaoyi3   

  1. 1. Department of Stomatology, Jinan Military General Hospital of Jinzhou Medical University, Jinan 250031, Shandong, China;
    2. School of Stomatology of Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan 250012, Shandong, China;
    3. Department of Stomatology, Jinan Military General Hospital, Jinan 250031, Shandong, China
  • Received:2015-09-22 Online:2016-09-10 Published:2016-09-10

摘要: 目的 探讨骨桥蛋白(OPN)在慢性睡眠剥夺(CSD)引起大鼠颞下颌关节(TMJ)结构变化中的作用。 方法 采用改良多平台法(MMPM)建立大鼠的慢性睡眠剥夺模型。 180只雄性Wistar大鼠随机分为2组:对照组(CON组)、慢性睡眠剥夺组(CSD组),每组90只。每组根据实验时间不同分为3个亚组:4、6、8周。通过HE染色观察大鼠TMJ的组织学结构变化;通过免疫组织化学染色检测OPN蛋白表达变化;通过免疫组织化学染色和免疫荧光检测NF-κB蛋白表达变化。 结果 CSD组的大鼠髁突均出现不同程度的病理变化,随着睡眠剥夺时间延长,软骨损伤更加严重。与CON组相比,CSD组OPN、NF-κB的蛋白表达水平明显升高(P<0.05),随睡眠剥夺时间延长,OPN、NF-κB表达均呈增加趋势。 结论 慢性睡眠剥夺能够激活大鼠颞下颌关节髁突软骨中软骨细胞及各种炎症细胞生成骨桥蛋白增多,OPN通过激活NF-κB通路,进而引起大鼠颞下颌关节发生病理性改变。

关键词: 慢性睡眠剥夺, 骨桥蛋白, 核转录因子kappaB, 颞下颌关节

Abstract: Objective To explore the effect of osteopontin(OPN)in the temporomandibular joint(TMJ)of rats subjected to chronic sleep deprivation(CSD). Methods Rats were subjected to CSD using the modified multiple platform method(MMPM). A total of 180 male 8-week-old Wistar rats were randomly divided into two groups(n=90 per group): the control(CON)group and chronic sleep deprivation(CSD)group. The two groups were equally divided into three subgroups(n=30 each)according to the observation time points(4, 6, and 8 weeks). The expression of OPN was measured with immunohistochemical method. The expression of NF-κB of TMJ was measured with immunohistochemical method and immunofluorescence. The relationship between the expressions of OPN and NF-κB and CSD extension was analyzed. Results Hematoxylin and eosin(HE)staining showed pathological alterations in the TMJ in the CSD group. With the extension of CSD, the injury on cartilage was exacerbated. The expressions of OPN and 山 东 大 学 学 报 (医 学 版)54卷9期 -丁凤,等.在慢性睡眠剥夺中骨桥蛋白通过NF-kappaB通路对颞下颌关节的影响 \=-NF-κB in the CSD groups were significantly higher than those in the control group(P<0.05). The expressions of OPN and NF-κB had a rising tendency with the extension of CSD. Conclusion CSD causes pathological alterations in the TMJ condylar cartilages by the expression of OPN from rat condylar cartilage chondrocytes and various inflammatory cells. OPN aggravates the pathological changes in the TMJ by activating the NF-κB signaling pathway.

Key words: Temporomandibular joint, Chronic sleep deprivation, Osteopontin, Nuclear factor-kappa B

中图分类号: 

  • R246.83
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