CAJ | 학술논문

目的：了解C反应蛋白（CRP）在强直性脊柱炎（AS）发病机制中的作用。方法体外培养AS滑膜成纤维细胞（ASFLS）。荧光定量聚合酶链反应（qRT-PCR）方法检测mRNA的表达，免疫组织化学法检测蛋白的表达。检测ASFLS中CRP及其受体CD32、CD64 mRNA和蛋白的表达。检测并比较在有无CRP刺激条件下，以及加入CD32拮抗剂前后ASFLS中各种炎症因子、基质金属蛋白酶（MMPs）的表达结果。结果 ASFLS中CRP及其受体CD32和CD64mRNA和蛋白表达均比正常滑膜细胞（HFLS）明显升高。与无CRP刺激相比，加入CRP刺激后ASFLS中各种炎症因子和MMPs表达明显升高（P<0.01）。加入CD32拮抗剂后CRP再刺激ASFLS各炎症因子和MMPs的mRNA表达比加入拮抗剂前明显减弱（P<0.01）。结论 CRP通过与受体CD32、CD64结合，上调各种炎症因子和MMPs的产生，加重AS的炎症破坏。CRP在AS中不仅是炎症标识因子，还可能参与了AS的发病发展。
목적：료해C반응단백（CRP）재강직성척주염（AS）발병궤제중적작용。방법체외배양AS활막성섬유세포（ASFLS）。형광정량취합매련반응（qRT-PCR）방법검측mRNA적표체，면역조직화학법검측단백적표체。검측ASFLS중CRP급기수체CD32、CD64 mRNA화단백적표체。검측병비교재유무CRP자격조건하，이급가입CD32길항제전후ASFLS중각충염증인자、기질금속단백매（MMPs）적표체결과。결과 ASFLS중CRP급기수체CD32화CD64mRNA화단백표체균비정상활막세포（HFLS）명현승고。여무CRP자격상비，가입CRP자격후ASFLS중각충염증인자화MMPs표체명현승고（P<0.01）。가입CD32길항제후CRP재자격ASFLS각염증인자화MMPs적mRNA표체비가입길항제전명현감약（P<0.01）。결론 CRP통과여수체CD32、CD64결합，상조각충염증인자화MMPs적산생，가중AS적염증파배。CRP재AS중불부시염증표식인자，환가능삼여료AS적발병발전。
Objective To investigate the effect of C-reactive protein (CRP) in the pathogenesis of ankylosing spondylitis (AS). Methods The AS synovial fibroblasts (ASFLS) were cultured in vitro. The expression level of mR-NA and protein was determined by quantitative real-time PCR (qRT-PCR) and immunohistochemical assay, respec-tively. The mRNA and protein expression levels of CRP and receptors CD32 and CD64 in ASFLS were determined. The expression levels of inflammatory factors and matrix metalloproteinases (MMPs) in ASFLS with/without CRP stimu-lation and CD32 antagonist were compared, respectively. Results The mRNA and protein expression levels of CRP and receptors CD32 and CD64 in ASFLS significantly increased compared with those in normal synoviocytes (HFLS). The expression levels of inflammatory factors and MMPs in ASFLS with CRP stimulation were significantly higher than those without CRP stimulation (P<0.01). The expression levels of inflammatory factors and MMPs in ASFLS with CD32 antagonist and CRP stimulation were significantly lower than those without CD32 antagonist (P<0.01). Conclusion By binding to receptors CD32 and CD64, CRP may up-regulate inflammatory factors and MMPs and increase inflammation in AS. CRP is not only an inflammatory biomarker, but also a mediator in the occurrence and development of AS.