目的 通過研究膠原誘導(dǎo)性關(guān)節(jié)炎大鼠肝組織基因表達譜，探討類風濕性關(guān)節(jié)炎的發(fā)病機制。方法 采用dChip（Dec.2009 version）分析軟件lower bound fold change方法分析表達差異1.5倍以上基因，芯片類型為GeneChip Rat Genome230，基因庫為Affymetrix Gene，參考GenBank基因庫，功能通路參考KEGG數(shù)據(jù)庫。用大鼠全基因表達譜芯片研究膠原誘導(dǎo)性關(guān)節(jié)炎及正常大鼠肝組織基因表達譜，比較模型大鼠及正常大鼠肝組織基因表達的差異。結(jié)果 結(jié)果顯示，膠原誘導(dǎo)性關(guān)節(jié)炎大鼠差異表達基因有1 009個，其中上調(diào)基因480個，下調(diào)基因529個。差異表達基因主要涉及生物過程調(diào)控、刺激反應(yīng)、細胞通信、細胞周期的負調(diào)控、免疫反應(yīng)、應(yīng)激反應(yīng)、血管生成、內(nèi)皮細胞分化等功能。涉及的代謝及信號通路主要有細胞凋亡通路、鈣調(diào)節(jié)通路、TGF-β通路、凝血功能通路、炎癥反應(yīng)通路等通路。模型組差異表達上調(diào)的基因主要有Aldh1a7、Bad、Gdf10、Ccar2、Slc1a3、Il1b、Il7、Vegfb、IgG-2a等，差異表達下調(diào)的基因主要有Ugt2b、Mx2、Usp18、Comt、Zfp354a、Oas1a、G1p2、Irf7等。結(jié)論 膠原誘導(dǎo)性關(guān)節(jié)炎是一個涉及多基因表達異常的全身免疫性疾病，篩選到的差異表達基因初步反映了類風濕關(guān)節(jié)炎的發(fā)病機制，為類風濕關(guān)節(jié)炎的防治提供重要線索。

Objective To better understand pathogenesis of rheumatoid arthritis (RA) and to facilitate the search for novel RA therapeutics, we studied collagen-induced arthritis rat hepatic tissue genes profile expression. Methods Using DNA microarray technology, the hepatic tissue genes profile expression of the collagen-induced arthritis rats and the normal rats was compared. Hepatic tissue was purified and total RNA was processed for a microarray analysis using Affymetrix Gene Chip technology. Statistical comparison analysis identified differentially expressed genes that distinguished CIA from control rats. Results Clustering analysis indicated that 1009 genes expression of rats with collagen-induced arthritis were differences compared with normal rats, including 480 up-regulated genes and 529 down-regulated genes. Differential genes involved in the function group of regulation of cellular process, stimulation, cell communication, vasculature development, immune response, inflammation, and the pathway of apoptosis, oxidative stress, blood clotting cascade, TGF Beta signaling pathway, and so on. The major overexpressed genes were Aldh1a7, Bad, Gdf10, Ccar2, Slc1a3, Il1b, Il7, Vegfb, and IgG-2a, and the major underexpressed genes were Ugt2b, Mx2, Usp18, Comt, Zfp354a, Oas1a, G1p2, and Irf7. Conclusion The collagen-induced arthritis is a systemic immune disease involving multi-genes abnormal expression. The abnormal genes could initially reflect the pathogenesis of rheumatoid arthritis, and provide important clues for the prevention and treatment of RA.