Cao Zhengming, Ding Xiaoquan, Huang Yuelong, Liu Songyang, Lin Jianhao, Lyu Houshan, Sun Tiezheng
Arthritis Clinic and Research Center, Peking University People's Hospital, Beijing 100044, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Apr;31(4):511-5, 519.
To observe the changes of synovial inflammation score and expression of related molecular markers in patients with rheumatoid arthritis treated with tumor necrosis factor (TNF) antagonist etanercept.
Sixteen patients with rheumatoid arthritis received synovectomy in the knee under arthroscopy, of which 8 patients had been treated with etanercept before surgery (etanercept group) and the other 8 patients were given no etanercept or other biologics (non-biological agent group). The synovial tissues obtained from surgery were subjected to HE staining and immunohistochemical staining respectively, to assess Rooney's inflammation score and detect the expressions of proliferating cell nuclear antigen (PCNA), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and cadherin-11.
Rooney's score in etanercept group was significantly lower than that in non-biological agent group. The expressions of PCNA and cadherin-11 in synovial lining and sublining layers significantly decreased in etanercept group. Expressions of VCAM-1 and ICAM-1 had no significant difference in either synovial lining or sublining layer between the two groups. Clinical inflammatory markers including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelet count (PLT) and disease activity score in 28 joints (DAS28) had no statistical correlation with Rooney's inflammation score.
Etanercept could effectively inhibit proliferation of synoviocytes and infiltration of lymphocytes in synovium of rheumatoid arthritis, and decrease the expressions of proliferation-and adhesion-related molecular markers, which histologically alleviated the synovial inflammation of rheumatoid arthritis. Clinical inflammatory markers might not fully reflect histological changes in the local synovial tissue.
观察肿瘤坏死因子（TNF）拮抗剂依那西普治疗类风湿关节炎患者时滑膜炎症评分及相关分子标志物表达的变化。
16例类风湿关节炎患者接受关节镜下膝关节滑膜切除术，其中8例患者术前接受依那西普治疗（依那西普组），另外8例患者未接受依那西普或其他生物制剂治疗（非生物制剂组）。分别对手术获取的滑膜组织进行苏木精-伊红（HE）染色和免疫组织化学染色，评估鲁尼炎症评分，并检测增殖细胞核抗原（PCNA）、血管细胞黏附分子-1（VCAM-1）、细胞间黏附分子-1（ICAM-1）和钙黏蛋白-11的表达。
依那西普组的鲁尼评分显著低于非生物制剂组。依那西普组滑膜衬里层和衬里下层中PCNA和钙黏蛋白-11的表达明显降低。两组滑膜衬里层或衬里下层中VCAM-1和ICAM-1的表达无显著差异。包括红细胞沉降率（ESR）、C反应蛋白（CRP）、血小板计数（PLT）和28个关节疾病活动评分（DAS28）在内的临床炎症标志物与鲁尼炎症评分无统计学相关性。
依那西普可有效抑制类风湿关节炎滑膜中滑膜细胞的增殖和淋巴细胞浸润，并降低增殖和黏附相关分子标志物的表达，从组织学上减轻类风湿关节炎的滑膜炎症。临床炎症标志物可能无法完全反映局部滑膜组织的组织学变化。
