Zhu Chunxia, Ji Yaoting, Liu Shengbo, Bian Zhuan
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University Wuhan 430079, Hubei, China.
Department of Endodontics, School and Hospital of Stomatology, Wuhan University Wuhan 430079, Hubei, China.
Am J Transl Res. 2016 Sep 15;8(9):3861-3871. eCollection 2016.
This study aimed to investigate whether follicle-stimulating hormone (FSH)-induced alveolar bone resorption was mediated by a cyclooxygenase 2 (COX-2) enzyme related mechanism. Experimental periodontitis was induced in bilateral ovariectomized (OVX) rats, some of which were injected with triptorelin, an FSH inhibitor. After mandibles were collected, we performed micro-computed tomography to evaluate alveolar bone loss and immunohistochemical staining to assess COX-2 expression. As well, human periodontal ligament cells (PDLCs) were treated with FSH (30 ng/ml), and the COX-2 mRNA and protein expression levels were measured by quantitative real-time polymerase chain reaction (qPCR) and Western blotting, respectively; prostaglandin E2 (PGE) levels were measured by enzyme-linked immunosorbent assay (ELISA). The results indicated that FSH significantly increased alveolar bone resorption and the expression of COX-2 in the bilateral OVX + Ligatured rats compared with the other treatment groups. FSH also increased the mRNA and protein expression of COX-2 and PGE (P < 0.01) in human PDLCs. Further, the analysis of signaling pathways revealed the activation of COX-2-mediated pathways including Erk, p38, and Akt. These data suggest that FSH aggravates alveolar bone loss via a COX-2-upregulation mechanism and that the Erk, p38, and Akt pathways are involved in this pathological process.
本研究旨在调查促卵泡激素（FSH）诱导的牙槽骨吸收是否由环氧化酶2（COX-2）相关机制介导。在双侧卵巢切除（OVX）大鼠中诱导实验性牙周炎，其中一些大鼠注射了FSH抑制剂曲普瑞林。收集下颌骨后，我们进行了显微计算机断层扫描以评估牙槽骨丢失情况，并进行免疫组织化学染色以评估COX-2表达。此外，用人牙周膜细胞（PDLCs）接受FSH（30 ng/ml）处理，分别通过定量实时聚合酶链反应（qPCR）和蛋白质印迹法测量COX-2 mRNA和蛋白质表达水平；通过酶联免疫吸附测定（ELISA）测量前列腺素E2（PGE）水平。结果表明，与其他治疗组相比，FSH显著增加了双侧OVX +结扎大鼠的牙槽骨吸收和COX-2表达。FSH还增加了人PDLCs中COX-2和PGE的mRNA和蛋白质表达（P < 0.01）。此外，信号通路分析揭示了包括Erk、p38和Akt在内的COX-2介导通路的激活。这些数据表明，FSH通过COX-2上调机制加重牙槽骨丢失，并且Erk、p38和Akt通路参与了这一病理过程。
