Expressions of interleukin-1 beta and matrix metalloproteinase-13 in articular cartilage and synovial fluid of osteoarthritis model in rabbits
10.7652/jdyxb201704008
- VernacularTitle:IL-1β和MMP-13在兔骨关节炎模型软骨和滑液中的表达
- Author:
Yuanxia HUANG
;
Haibin XU
;
Chun GUO
- Keywords:
osteoarthritis;
articular cartilage;
synovial fluid;
IL-1β;
MMP-13
- From:
Journal of Xi'an Jiaotong University(Medical Sciences)
2017;38(4):507-511,528
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the feasibility of osteoarthritis (OA) model in rabbits by injuring medial meniscus so as to understand the role of interleukin-1 beta (IL-1β) and matrix metalloproteinase-13 (MMP-13) in pathological mechanism of articular cartilage and synovial fluid of OA model in rabbits.Methods We randomly divided 40 New Zealand white rabbits into experimental group (n =30) and control group (n =10).Pathological changes in articular cartilage of the femoral condyle were scored at weeks 2,6 and 12 after surgery.We detected the expressions of IL-1β and MMP-13 by immunohistochemistry.The cell fractions of IL-1β and MMP-13 were recorded by ELISA.Results The articular cartilage score and HE staining significantly differed at various time points of gross and pathological observation between control group and experimental group (P＜ 0.05).Immunohistochemistry showed that IL-1β was expressed in both groups and that the cell fraction differed significantly at weeks 6 and 12 (P＜0.05),but not at week 2 between the two groups.MMP-13 protein expression was not detected in articular condrocytes in control group,but was detected in experiment group with a significant difference (P＜0.05).IL-1β expression was consistent in articular cartilage and synovial fluid.Conclusion The reasonable rabbit animal OA model could be established by knee meniscus injury caused by surgical method.Expressions of IL-1β and MMP-13 change obviously in the pathomechanism of OA.Further clinical studies are needed to determine whether they can be used as markers in early diagnosis of OA.
