上海口腔医学 ›› 2022, Vol. 31 ›› Issue (2): 148-155.doi: 10.19439/j.sjos.2022.02.007

• 论著 • 上一篇    下一篇

慢性睡眠剥夺对大鼠髁突软骨的影响

白月辉1, 刘阳1, 崔玉兰1,2,3, 姜杉杉1, 商庆龙1, 赵琛1,2,3   

  1. 1.河北医科大学口腔医学院·口腔医院 修复科,河北 石家庄 050017;
    2.河北省口腔医学重点实验室,河北 石家庄 050017;
    3.河北省口腔疾病临床医学研究中心,河北 石家庄 050017
  • 收稿日期:2021-08-26 修回日期:2021-11-09 出版日期:2022-04-25 发布日期:2022-05-16
  • 通讯作者: 赵琛,E-mail:zhaochen36@163.com
  • 作者简介:白月辉(1993-),男,在读硕士研究生,E-mail:673303736@qq.com
  • 基金资助:
    河北省财政厅老年病防治项目(361029); 河北省医学科学研究课题计划(20201193); 河北省重点研发计划(17277761D)

Effect of chronic sleep deprivation on condylar cartilage in rats

BAI Yue-hui1, LIU Yang1, CUI Yu-lan1,2,3, JIANG Shan-shan1, SHANG Qing-long1, ZHAO Chen1,2,3   

  1. 1. Department of Prosthodontics, School and Hospital of Stomatology, Hebei Medical University. Shijiazhuang 050017;
    2. Hebei Key Laboratory of Stomatology. Shijiazhuang 050017;
    3. Hebei Clinical Research Center For Oral Disease Hebei Medical University. Shijiazhuang 050017, Hebei Province, China
  • Received:2021-08-26 Revised:2021-11-09 Online:2022-04-25 Published:2022-05-16

摘要: 目的: 建立大鼠慢性睡眠剥夺模型,观察大鼠颞下颌关节髁突软骨形态变化和软骨中IL-1β、TNF-α、IGF-1和VEGF的表达变化。方法: 将60只大鼠随机分为实验组、对照组和恢复组。利用改良多平台法(modified multiple platform method,MMPM)对实验组和恢复组大鼠进行1、2、3、4周的慢性睡眠剥夺。恢复组大鼠睡眠剥夺后正常笼养1周。利用H-E染色观察颞下颌关节髁突的组织结构变化,免疫组织化学法检测IL-1β、TNF-α、IGF-1和VEGF在髁突软骨内的表达水平。采用SPSS 23.0软件包对数据进行统计学分析。结果: 改良水平台法可以成功建立大鼠慢性睡眠剥夺模型。H-E染色观察到实验组髁突软骨出现纤维带分裂、细胞界限模糊,恢复组纤维裂隙减小或被纤维样组织占据。免疫组织化学结果显示,IL-1β、TNF-α在实验组中的阳性表达显著高于对照组(P<0.05),恢复组表达显著低于实验组(P<0.05)。IGF-1和VEGF在实验组中的表达显著高于对照组(P<0.05),恢复组1、2、3周IGF-1和VEGF的阳性表达显著下降(P<0.05)。结论: 慢性睡眠剥夺可引起髁突软骨内IL-1β、TNF-α、VEGF的表达增加,加重炎症表现。慢性睡眠剥夺可导致髁突软骨内IGF-1表达增加,发挥保护和促进软骨改建的作用。慢性睡眠剥夺停止1周后,各因子表达有所下降,髁突进行恢复性改建。

关键词: 慢性睡眠剥夺, 白细胞介素1β, 肿瘤坏死因子α, 胰岛素样生长因子1, 血管内皮细胞生长因子

Abstract: PURPOSE: The aim of this study was to investigate the morphological changes of condylar cartilage of temporomandibular joint (TMJ) and the expression changes of IL-1β,TNF-α,IGF-1 and VEGF in condylar cartilage of TMJ by establishing a chronic sleep deprivation model in rats. METHODS: Sixty rats were randomly divided into experimental group, control group and recovery group. Modified multiple platforms method (MMPM) was used to build chronic sleep deprivation models in experimental and recovery groups. Rats in the recovery group received 1 week of cage feeding after sleep deprivation. H-E staining was used to observe morphological change of the condyle. Immunohistochemical method was performed to detect the changes of IL-1β, TNF-α, IGF-1 and VEGF. The data was processed by using SPSS 23.0 software package. RESULTS: MMPM can establish chronic sleep deprivation model effectively. H-E staining showed condylar cartilage of the experimental group was split stripped, and the boundaries of cartilage cell layer became blurred. Compared with the control group, the recovery group had less cracks in the fibrous layer or some of the cracks were occupied by fibrous tissue. Immunohistochemistry showed that the positive expression intensity of IL-1β and TNF-α in the experimental group was significantly higher than in the control group (P<0.05), the positive expression intensity in the recovery group was significantly lower than in the experimental group(P<0.05). The positive expression intensity of IGF-1 and VEGF in the experimental group was significantly higher than in the control group(P<0.05). The expression of IGF-1 and VEGF decreased significantly in the recovery group which received sleep deprivation no more than 3 weeks(P<0.05). CONCLUSIONS: Chronic sleep deprivation can increase the expression of IL-1β, TNF-α and VEGF in condylar cartilage and aggravate osteoarthritis. Chronic sleep deprivation can lead to increase of IGF-1 in condylar cartilage tissue, which plays a crucial role in protecting and promoting the reconstruction of condylar cartilage. After chronic sleep deprivation, the expressions of IL-1β, TNF-α, IGF-1 and VEGF in the condylar cartilage of rats were decreased after 1 week of recovery, and the condylar cartilage underwent restorative reconstruction.

Key words: Chronic sleep deprivation, Interleukin-1β, Tumor necrosis factor α, Insulin-like growth factor, Vascular endothelial growth fact

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