CAJ | 학술논문

目的观察TLR2配体肽聚糖(PGN)刺激对低氧诱导类风湿关节炎滑膜成纤维细胞(RASF)表达低氧诱导因子1 α(HIF-1 α)和血管内皮生长因子(VEGF)的影响.方法分离RASF 6例,建立体外培养体系,将RASF分为对照组、CoCl2组、PGN组和CoCl2+PGN组,qRT-PCR检测HIF-1 α表达,ELISA检测VEGF表达,siHIF-1 α后ELISA检测VEGF表达.结果 CoCl2组RASF表达HIF-1 α和VEGF水平高于对照组(P＜0.05),PGN刺激能明显增强CoGl2诱导RASF表达HIF-1 α和VEGF的水平(P＜0.05),干扰HIF-1 α后明显下调PGN协同CoCl2诱导RASF产生VEGF的效应(P＜0.05).结论 TLR2信号激活能明显增强低氧诱导RASF产生VEGF的能力,干扰HIF-1 α是RA治疗的有效策略.
목적 관찰TLR2배체태취당(PGN)자격대저양유도류풍습관절염활막성섬유세포(RASF)표체저양유도인자1 α(HIF-1 α)화혈관내피생장인자(VEGF)적영향.방법 분리RASF 6례,건입체외배양체계,장RASF분위대조조、CoCl2조、PGN조화CoCl2+PGN조,qRT-PCR검측HIF-1 α표체,ELISA검측VEGF표체,siHIF-1 α후ELISA검측VEGF표체.결과 CoCl2조RASF표체HIF-1 α화VEGF수평고우대조조(P＜0.05),PGN자격능명현증강CoGl2유도RASF표체HIF-1 α화VEGF적수평(P＜0.05),간우HIF-1 α후명현하조PGN협동CoCl2유도RASF산생VEGF적효응(P＜0.05).결론 TLR2신호격활능명현증강저양유도RASF산생VEGF적능력,간우HIF-1 α시RA치료적유효책략.
Objective To investigate the effect of peptidoglycan (PGN) on the expression of hypoxia-inducible factor-1 α (HIF-1 α) and vascular endothelial growth factor (VEGF) in rheumatoid arthritis synovial fibroblast (RASF) induced by hypoxia.Methods RASF were isolated from 6 cases of rheumatoid arthritis (RA) and cultured in vitro,then divided into control group,CoCl2 group,PGN group and CoCl2 + PGN group.The mRNA level of HIF-1 α was detected by qRT-PCR and then the protein level of VEGF was tested by ELISA before and after silencing HIF-1 α.Results The expression of HIF-1 α and VEGF was upregulated in RASF induced by CoCl2 compared to control (P ＜ 0.05).PGN potentiated the levels of HIF-1 α and VEGF in RASF treated by CoCl2 (P ＜ 0.05).Silencing HIF-1 α decreased PGN and hypoxia-augmented VEGF production (P ＜ 0.05).Conclusion Activation of TLR2 signaling can enhance the levels of HIF-1 α and VEGF in RASF under hypoxia environment,and interfereing of HIF-1 α may be an effective therapeutic strategy for RA.