Zhang Chen, Liu Jun, Yuan Changqing, Ji Qiuxia, Chen Daiyun, Zhao Han, Jiang Weijie, Ma Kangjie, Liu Lingshuang
Department of Stomatology, Affiliated Hospital of Qingdao University Qingdao, P. R. China.
Qingdao University Qingdao, P. R. China.
Int J Clin Exp Pathol. 2019 Jan 1;12(1):190-197. eCollection 2019.
It has been shown that JAK2/STAT3 is involved in the occurrence of various inflammatory diseases. The purpose of this study was to associate the expression of Janus kinase 2 (JAK2) and its receptor signal transducer and activator of transcription 3 (STAT3) and suppressors of cytokine signaling 3 (SOCS3), to periapical granuloma.
Samples were collected from 40 patients who were divided into two groups, namely, healthy control (N=20) and periapical granuloma (N=20) groups in accordance with classified standards. The samples were prepared for histological analysis, immunohistochemistry, and double immunofluorescence staining.
Only slight inflammatory cell infiltration was observed in the tissues from the healthy control group. Extensive infiltration of inflammatory cells was observed in patients with chronic periapical disease. The periapical granuloma group had higher levels of JAK2, STAT3, p-JAK2, p-STAT3 and SOCS3 (all P<0.05) than the control group. Double immunofluorescence staining results showed the presence of JAK2-positive and STAT3-positive cells in the periapical lesion areas.
This study demonstrated that JAK2, STAT3, and SOCS3 can be observed and may be associated with the inflammatory process in periapical lesions. The results of this study will provide new insights into the pathological mechanisms of human periapical granuloma.
已有研究表明JAK2/STAT3参与多种炎症性疾病的发生。本研究旨在探讨牙合面肉芽肿中Janus激酶2(JAK2)及其受体信号转导和转录激活因子3(STAT3)以及细胞因子信号转导抑制因子3(SOCS3)的表达情况。
收集40例患者的样本,根据分类标准将其分为两组,即健康对照组(N=20)和牙合面肉芽肿组(N=20)。对样本进行组织学分析、免疫组织化学和双重免疫荧光染色。
健康对照组组织中仅观察到轻微的炎症细胞浸润。慢性根尖周病患者中观察到广泛的炎症细胞浸润。牙合面肉芽肿组的JAK2、STAT3、p-JAK2、p-STAT3和SOCS3水平均高于对照组(均P<0.05)。双重免疫荧光染色结果显示根尖周病变区域存在JAK2阳性和STAT3阳性细胞。
本研究表明JAK2、STAT3和SOCS3可被观察到,并且可能与根尖周病变的炎症过程有关。本研究结果将为人类牙合面肉芽肿的病理机制提供新的见解。