摘要
目的通过比较胶原诱导(CIA)和人肿瘤坏死因子α转基因(hTNFα-Tg)小鼠关节炎模型的临床特征,为炎症性关节炎疾病的致病机理和药物筛选研究提供合适的模式动物。方法分别采用鸡Ⅱ型胶原注射DBA/1小鼠建立经典的类风湿性关节炎(RA)模型,利用人肿瘤坏死因子α注射FVB小鼠建立关节炎转基因小鼠模型,通过关节表观特征观察、关节炎指数分析和病理观察评分对炎症性关节炎模型进行评价。结果在炎症细胞浸润方面,CIA模型主要有中性粒细胞浸润,hTNFα-Tg模型主要是淋巴细胞浸润,且差异有统计学意义(P<0.05);在细胞增殖方面,两种模型都显示滑膜细胞的增生,与CIA模型相比,hTNFα-Tg模型滑膜增生最为严重,差异有统计学意义(P<0.05);在骨侵蚀方面,两种模型都显示增生滑膜对骨的侵蚀,两种模型比较,差异无统计学意义(P>0.05)。结论两种关节炎模型均在一定程度上模拟人关节炎的临床症状,但也存在着差异。CIA模型造模时间长,能较好模拟RA临床特征;hTNFα-Tg模型属于自发型,表现为滑膜不断增生,符合RA晚期临床特征。
Objective To compare the arthritis features between collagen-induced arthritis（ CIA） mice and human tumor necrosis factor alpha transgenic（ hTNFa-Tg） mice,providing appropriate animal models for pathogenesis analysis and drug screening of inflammatory arthritis diseases. Methods The inflammatory arthritis in mice were induced by collagen emulsion and human tumor necrosis factor-α gene transfection,which was evaluated, through the joint appearance observation, arthritis index score analysis and pathological observation. Results The pathological score of study,compared with the CIA model,hTNFα-Tg model was the most serious in synovial hyperplasia,that there was statistical difference（ P〈0.05）; in the infiltration of inflammatory cells,CIA model mainly neutrophil infiltration and hTNFα-Tg model is mainly lymphocytic infiltration,and there was a statistical difference（ P〈0.05）; inbone erosion,between CIA model and hTNFα-Tg model,there was no statistical difference（ P〈0.05）. Conclusion The clinical symptoms of two arthritis arthritis models are simulated in a certain extent,and there are also differences between the CIA model which can well simulate the clinical characteristics of rheumatoid arthritis and hTNFα-Tg model which belongs to spontaneity,shows synovial proliferation and is consistent with clinical features advanced RA.
出处
《广东药科大学学报》
CAS
2017年第3期366-370,共5页
Journal of Guangdong Pharmaceutical University
基金
广东省科技计划项目(2013B060300025
2015A030303006
2014A030304029
2016A030303022)
关键词
关节炎
小鼠模型
胶原诱导
人肿瘤坏死因子Α
炎症
arthritis
mouse model
collagen-induced
human tumor necrosis factor α
inflammation
