异常应力对MIF、COX2和PGE2在颞下颌关节骨关节炎中的促进作用及其机制
Effects and mechnism of abnormal stress promoting MIF, COX2 and PGE2 in the progression of temporomandibular joint osteoarthritis
- 解放军医学杂志 2023年48卷第11期 页码：1294-1304
- 作者机构：
1.新疆医科大学第一附属医院(附属口腔医院)口腔颌面肿瘤外科，新疆乌鲁木齐 830054
2.新疆维吾尔自治区口腔医学研究所，新疆乌鲁木齐 830054
- 作者简介：
许颖捷，医学博士，住院医师，主要从事颞下颌关节骨关节炎方面的研究
龚忠诚，E-mail：gump0904@aliyun.com
- 基金信息：国家自然科学基金(82160189);新疆维吾尔自治区“天山创新团队计划”(2021D14001);自治区研究生创新项目(XJ2021G191)
DOI：10.11855/j.issn.0577-7402.0916.2023.0919
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许颖捷, 童乔莹, 尚婷荷, 等. 异常应力对MIF、COX2和PGE2在颞下颌关节骨关节炎中的促进作用及其机制[J]. 解放军医学杂志, 2023, 48(11): 1294-1304.
Xu Ying-Jie,Tong Qiao-Ying,Shang Ting-He,et al.Effects and mechnism of abnormal stress promoting MIF, COX2 and PGE2 in the progression of temporomandibular joint osteoarthritis[J].Medical Journal of Chinese People′s Liberation Army,2023,48(11):1294-1304.
许颖捷, 童乔莹, 尚婷荷, 等. 异常应力对MIF、COX2和PGE2在颞下颌关节骨关节炎中的促进作用及其机制[J]. 解放军医学杂志, 2023, 48(11): 1294-1304. DOI： 10.11855/j.issn.0577-7402.0916.2023.0919.
Xu Ying-Jie,Tong Qiao-Ying,Shang Ting-He,et al.Effects and mechnism of abnormal stress promoting MIF, COX2 and PGE2 in the progression of temporomandibular joint osteoarthritis[J].Medical Journal of Chinese People′s Liberation Army,2023,48(11):1294-1304. DOI： 10.11855/j.issn.0577-7402.0916.2023.0919.
摘要
目的,2,探讨异常应力对巨噬细胞移动抑制因子(MIF)、环氧合酶2(COX2)和前列腺素E2(PGE2)在颞下颌关节骨关节炎(TMJOA)中的促进作用及其机制。,方法,2,收集2020年1月－2021年12月就诊于新疆医科大学第一附属医院颞下颌关节专病门诊并伴有错,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405433&type=,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405437&type=,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405434&type=,3.22321177,3.03334355,3.175,的30例TMJOA患者(TMJOA组，根据分期分为TMJOA Ⅰ期、Ⅱ期、Ⅲ期，,n,=10)及30例颞下颌关节结构内紊乱病(TMJID)患者(TMJID组)，采用视觉模拟评分评价各组患者咬合状态时的疼痛评分，采用ELISA检测各组滑液中MIF、COX2和PGE2的表达水平。将单侧前牙反,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405431&type=,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405450&type=,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405449&type=,3.22321177,3.03334355,3.175,(UAC)TMJOA模型大鼠分别处理4、8、12周(分别为UAC-4周组、UAC-8周组和UAC-12周组，,n,=6)，同时设置相应的对照组(Ctrl-4周组、Ctrl-8周组和Ctrl-12周组，,n,=6，未做处理，饲养条件与UAC组一致)。采用ELISA检测各组大鼠血清和关节滑液中MIF、COX2和PGE2的表达水平，采用Western blotting检测各组大鼠颞下颌关节中白细胞介素(IL)-1β、IL-18、MIF、COX2和PTGER2的表达水平。建立滑膜成纤维样细胞(FLSs)的流体流动剪切应力(FFSS)模型并分为对照组(0 dyn/cm,2, FFSS)与1、3、5、10 dyn/cm,2, FFSS组，采用RT-PCR和Western blotting检测上述指标mRNA和蛋白的表达水平。,结果,2,视觉模拟评分评价显示，TMJOA Ⅰ、Ⅱ期患者疼痛评分明显高于TMJID患者(,P,<,0.001)；ELISA检测结果显示，TMJOA组关节滑液MIF、COX2和PGE2表达水平明显高于TMJID组(,P,<,0.05)，且在TMJOA Ⅱ期组表达水平最高。大鼠TMJOA模型中，与相应的对照组比较，UAC-4、8、12周组的血清和关节滑液中MIF、COX2和PGE2表达水平增高，且在UAC-8周时明显增高(,P,<,0.05)；与对照组比较，UAC组颞下颌关节组织中IL-1β、IL-18、MIF、COX2和PTGER2蛋白的表达水平也明显升高(,P,<,0.05)。FFSS干预FLSs的细胞模型中，随着FFSS的增大，细胞发生形变、胞膜不完整，且细胞数量减少；与对照组比较，1、3、5、10 dyn/cm,2,干预组FLSs的IL-1β、IL-18、MIF、COX2和PGE2(PTGER2)的表达水平明显升高(,P,<,0.05)。,结论,2,MIF、COX2、PGE2在伴有错,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405452&type=,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405455&type=,https://html.publish.founderss.cn/rc-pub/api/common/picture?pictureId=51405447&type=,3.22321177,3.03334355,3.175,畸形的TMJOA患者颞下颌关节滑液及UAC大鼠血清及关节滑液中高表达，异常流体流动剪切应力可促进FLSs分泌MIF、COX2、PGE2，参与关节微环境炎症，从而加速疾病的进展。
Abstract
Objective,2,To investigate the effects and mechnism of abnormal stress promoting macrophage mobility inhibitory factor (MIF), cyclooxygenase 2 (COX2) and prostaglandin E2 (PGE2) in the progression of temporomandibular joint osteoarthritis (TMJOA).,Methods,2,From January 2020 to December 2021, TMJOA and temporomandibular joint internal derangement (TMJID) patients (30 cases in each group, we divided the TMJOA into group TMJ Ⅰ, Ⅱ, Ⅲ according to the stage) who were admitted to TMJOA special clinic of the First Affiliated Hospital of Xinjiang Medical University and accompanied by abnormal occlusion were collected. The pain score of the occlusal state of the patients was evaluated by visual analogue scale. The expression levels of MIF, COX2 and PGE2 in synovial fluid were detected by ELISA. We used the unilateral anterior crossbite for TMJOA (UAC) rats model (the grouped into: UAC-4 weeks, UAC-8 weeks and UAC-12 weeks group), and control group at the same time (grouped into: Ctrl-4 weeks, Ctrl-8 weeks and Ctrl-12 weeks group), each group had 6 rats. The expression levels of MIF, COX2 and PGE2 in serum and synovial fluid of rats were detected by ELISA. The expression levels of IL-1β, IL-18, MIF, COX2 and PTGER2 in temporomandibular joint of rats were detected by Western blotting. The fluid flow shear stress (FFSS) model of fibroblast-like synovial cells (FLSs) was established, and the mRNA and protein expression levels of above indexes were detected by RT-PCR and Western blotting.,Results,2,Visual analogue scale evaluation showed that the pain score of TMJOA Ⅰ and Ⅱ group was significantly higher than that of TMJID (,P,<,0.001). ELISA results showed that the expression levels of MIF, COX2 and PGE2 in synovial fluid in TMJOA group were higher than those in TMJID group (,P,<,0.05), and the expression levels were the highest in TMJOA Ⅱ group. Compared with control group, the expressions of MIF, COX2 and PGE2 in serum and synovial fluid at UAC-4 weeks, 8 weeks and 12 weeks were slightly higher, and significantly higher at UAC-8 weeks in rat TMJOA model (,P,<,0.05). In addition, the expression trend of protein levels in temporomandibular joint tissues was similar, which showed higher expression levels of IL-1β, IL-18, MIF, COX2 and PTGER2 (,P,<,0.05). In the cell model where FFSS interfered with FLSs, with the increase of FFSS, cell with deformation, incomplete cell membrane and reduced number. Compared with control group, the expression levels of IL-1β, IL-18, MIF, COX2 and PGE2 (PTGER2) of FLSs were increased in 1, 3, 5 and 10 dyn/cm,2, intervention groups (,P,<,0.05).,Conclusion,2,MIF, COX2 and PGE2 were highly expressed in temporomandibular joint synovial fluid of TMJOA patients with malocclusion. And these three factors were also highly expressed in serum and synovial fluid of UAC rats. The abnormal fluid shear stress promotes the secretion of MIF, COX2 and PGE2 by FLSs to participate in joint microenvironment inflammation and accelerate disease progression.
关键词
颞下颌关节骨关节炎巨噬细胞移动抑制因子异常应力滑膜疼痛
Keywords
temporomandibular joint osteoarthritismacrophage mobility inhibitory factorabnormal stresssynovialpain
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