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碧萝芷调节血管内皮生长因子（VEGF）和基质金属蛋白酶组织抑制因子-1（TIMP-1）的产生，并降低类风湿性关节炎滑膜细胞的侵袭性。

Piascledine modulates the production of VEGF and TIMP-1 and reduces the invasiveness of rheumatoid arthritis synoviocytes.

作者信息

Cinelli M, Guiducci S, Del Rosso A, Pignone A, Del Rosso M, Fibbi G, Serratì S, Gabrielli A, Giacomelli R, Piccardi N, Matucci Cerinic M

机构信息

Department of Medicine and Surgery, Division of Medicine and Rheumatology, AOUC, University of Florence, Italy.

出版信息

Scand J Rheumatol. 2006 Sep-Oct;35(5):346-50. doi: 10.1080/03009740600709865.

DOI:10.1080/03009740600709865

PMID:17062432

Abstract

BACKGROUND

In rheumatoid arthritis (RA), hypertrophy of the synovial membrane generates a tumour-like pannus that invades the joint cavity and erodes cartilage and bone. Invasion of the extracellular matrix (ECM) is accompanied by angiogenesis, in which vascular endothelial growth factor (VEGF) and tissue inhibitors of metalloproteinases (TIMPs), produced by synoviocytes lining the pannus, have a primary role. Piascledine (PSD) is used in the treatment of osteoarthritis and has anti-inflammatory effects in vitro.

OBJECTIVE

To study the effects of PSD on levels of VEGF and TIMP-1 and chemoinvasion in RA synoviocytes and healthy controls.

METHODS

The effects of PSD 5, 10, and 20 microg/mL were evaluated, with/without interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNFalpha) 20 ng/mL, on synoviocytes. The levels of VEGF and TIMP-1 were assayed in the culture medium by enzyme-linked immunosorbent assay (ELISA). Chemoinvasion was measured by the Boyden chamber invasion assay.

RESULTS

RA synoviocytes treated with PSD showed, compared to basal, lower levels of VEGF (41080+/-830 vs. 79210+/-920 pg/106 cells, p<0.001) and increased levels of TIMP-1 (23540+/-93.2 vs. 12860+/-42.9 ng/106 cells, p<0.001). PSD decreased dose-dependently IL-1beta and TNFalpha induced migration.

CONCLUSIONS

In RA synoviocytes, and also to a lesser extent in control cells, PSD modulates VEGF and TIMP-1 and decreases chemoinvasion. PSD might have a role in the treatment of RA synovitis controlling invasiveness.

摘要

背景

在类风湿关节炎（RA）中，滑膜肥大产生肿瘤样血管翳，其侵入关节腔并侵蚀软骨和骨。细胞外基质（ECM）的侵入伴随着血管生成，其中血管内皮生长因子（VEGF）和基质金属蛋白酶组织抑制剂（TIMPs）由血管翳内衬的滑膜细胞产生，起主要作用。吡西卡尼（PSD）用于治疗骨关节炎，在体外具有抗炎作用。

目的

研究PSD对RA滑膜细胞和健康对照中VEGF和TIMP-1水平以及化学侵袭的影响。

方法

评估5、10和20μg/mL的PSD在有/无20 ng/mL白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNFα）情况下对滑膜细胞的作用。通过酶联免疫吸附测定（ELISA）检测培养基中VEGF和TIMP-1的水平。通过Boyden小室侵袭试验测量化学侵袭。

结果

与基础水平相比，用PSD处理的RA滑膜细胞中VEGF水平较低（41080±830 vs. 79210±920 pg/106细胞，p<0.001），TIMP-1水平升高（23540±93.2 vs. 12860±42.9 ng/106细胞，p<0.001）。PSD剂量依赖性地降低IL-1β和TNFα诱导的迁移。