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  

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

作　　者：丁凤[1] 董亚兵[2] 赵华强[2] 朱国雄[3] 吴高义[3] 

机构地区：[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

出　　处：《山东大学学报（医学版）》2016年第9期41-47,58,共8页Journal of Shandong University:Health Sciences

基　　金：国家自然科学基金(81400573)

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。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 irnmunohistochemical method. The expression of NF-KB of TMJ was measured with immunohistochemical method and immunofluorescence. The relationship between the expressions of OPN and NF-KB 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 NF-KB in the CSD groups were significantly higher than those in the control group （ P 〈 0.05 ）. The expressions of OPN and NF-KB 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-KB signaling pathway.

关 键 词：慢性睡眠剥夺 颞下颌关节 骨桥蛋白 核转录因子kappa B 

分 类 号：R246.83[医药卫生—针灸推拿学]