摘要目的：探讨IL-34对RA患者成纤维样滑膜细胞（FLS）前列腺素E2（PGE2）/环氧化酶2（COX-2）表达的影响。方法分离培养6例RA患者FLS，分别用IL-34（50 ng/ml）、IL-34受体拮抗剂（25 ng/ml）加IL-34（50 ng/ml）、信号通路抑制剂（10μmol/L）加IL-34（50 ng/ml）刺激。采用反转录（RT）-PCR 检测FLS Cox2 mRNA表达；用ELISA 检测细胞培养上清中PGE2水平。2组间比较采用t检验。结果与未刺激组相比，IL-34刺激FLS后COX-2和PGE2水平增高，以48 h最为明显[（139±24） pg/ml和（201±8） pg/ml，t=-6.177，P＜0.01]；且加入IL-34受体拮抗剂刺激FLS 24、48、74 h，均可使IL-34刺激的RA FLS分泌PGE2水平降低[（250±58） pg/ml和（100±28） pg/ml，t=5.742，P＜0.01；（375±24） pg/ml和（97±23） pg/ml，t=20.564，P＜0.01；（357±21） pg/ml和（94±18） pg/ml，t=22.353，P＜0.01]；此外，细胞培养体系中加入NF-κB和P38 MAPK抑制剂后，IL-34刺激RA FLS产生PGE2水平明显下降[（279±37） pg/ml和（63±17） pg/ml，t=12.806，P＜0.01；（279±37） pg/ml和（77±16） pg/ml，t=6.177，P＜0.01]。结论 IL-34与其受体结合可能通过NF-κB和P38 MAPK信号通路促进RA FLS分泌PGE2，提示其可能参与RA的发病。

abstractsObjective To investigate the effects of interleukin-34 (IL-34) on prostaglandin E2 (PGE2)/cyclo-oxygenase-2 (COX-2) expression on fibroblast-like synoviocytes (FLS) in patients with rheumatoid arthritis (RA). Methods FLS was isolated from 6 RA patients and stimulated with IL-34 (50 ng/ml), IL-34 receptor antagonist (25 ng/ml) and IL-34 (50 ng/ml), inhibitors of signaling pathway (10 μmol/L) and IL-34 (50 ng/ml) in vitro respectively. The expression of COX-2 mRNA was detected by reverse transcription polymerase chain reac-tion (RT-PCR). The level of PGE2 in the supernatant of RA FLS culture was measured by Enzyme linked immunosorbent assay (ELISA). Statistical analysis between groups were performed by t test. Results Com-pared to unstimulated FLS, COX-2 and PGE2 expression was increased dramatically on IL-34-stimulated FLS, most evidently in 48 hours [(139±24) pg/ml vs (201±8) pg/ml, t=-6.177, P<0.01]; Moreover, the level of PGE2 was decreased when anti-IL-34 antibody was added to the IL-34-stimulated RA FLS at 24 hours, 48 hours, 72 hours [(250 ±58) pg/ml vs (100 ±28) pg/ml, t=5.742, P<0.01; (375 ±24) pg/ml vs (97 ±23) pg/ml, t=20.564, P<0.001; (357 ±21) pg/ml vs (94 ±18) pg/ml, t=22.353, P<0.01]; In the presence of SB203580 and IKK-16, PGE2 level produced by IL-34-stimulated FLS was obviously decreased [(279 ±37) pg/ml vs (63 ±17) pg/ml, t=12.806, P<0.01;(279±37) pg/ml vs (77±16) pg/ml, t=6.177, P<0.01]. Conclusion Binding of IL-34 with its&nbsp;receptor may promote the secretion of PGE2 via NF-κB and P38 MAPK signaling pathway in RA FLS, suggesting that it might be involved in the pathogenesis of RA.