The effect of anti-inflammatory and antifibrotic agents on fibroblasts obtained from arthrofibrotic tissue

Bone & Joint Research

article

X. Tang¹  S. Teng¹  M. Petri¹  C. Krettek¹  C. Liu¹  M. Jagodzinski¹ 

[1] Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology

关键词: Arthrofibrosis;    Anti-inflammation;    Antifibrosis;    Proliferation;    Differentiation;   

DOI  :  10.1302/2046-3758.73.BJR-2017-0219.R2

学科分类：骨科学

来源: British Editorial Society Of Bone And Joint Surgery

【 摘 要 】

ObjectivesThe aims of this study were to determine whether the administration of anti-inflammatoryand antifibrotic agents affect the proliferation, viability, and expression of markers involvedin the fibrotic development of the fibroblasts obtained from arthrofibrotic tissue in vitro, andto evaluate the effect of the agents on arthrofibrosis prevention in vivo.MethodsDexamethasone, diclofenac, and decorin, in different concentrations, were employedto treat fibroblasts from arthrofibrotic tissue (AFib). Cell proliferation was measured byDNA quantitation, and viability was analyzed by Live/Dead staining. The levels of procollagen type I N-terminal propeptide (PINP) and procollagen type III N-terminal propeptide(PIIINP) were evaluated with enzyme-linked immunosorbent assay (ELISA) kits. In addition, the expressions of fibrotic markers were detected by real-time polymerase chain reaction (PCR). Fibroblasts isolated from healthy tissue (Fib) served as control. Further, a rabbitmodel of joint contracture was used to evaluate the antifibrotic effect of the three differentagents.ResultsDexamethasone maintained the viability and promoted the proliferation of AFib. Diclofenacdecreased the viability and inhibited the cell proliferation during the first week of cultivation. However, decorin inhibited AFib proliferation and downregulated the expressionsof fibrotic markers. Additionally, decorin could improve the flexion contracture angle andinhibit the deposition of interstitial matrix components in the rabbit joint model.ConclusionDecorin decreased the expression of myofibroblast markers in AFib, inhibited the proliferation of AFib, and prevented the initial procedure of arthrofibrosis in vivo, suggesting thatdecorin could be a promising treatment to inhibit the development of arthrofibrosis.

【 授权许可】

CC BY-NC