摘要
目的 :研究外源性炎症因子白细胞介素 1β(interleukin 1β,IL 1β)对颞下颌关节骨关节病与正常髁突软骨细胞代谢活动的影响 ,探讨其在颞下颌关节骨关节病进展过程中所发挥的作用。方法 :采用 2 0 μg·L-1重组白介素1β(recombinedhumaninterleukin 1β ,rhIL 1β)刺激体外贴壁培养条件下的成兔正常成熟髁突软骨细胞与兔实验性颞下颌关节骨关节病模型髁突软骨细胞 ,RT PCR方法检测、比较细胞对软骨基质成分Ⅱ型胶原、蛋白多糖聚糖体、胶原酶以及内源性生长因子胰岛素样生长因子 1(insulin likegrowthfactor 1,IGF 1)和转移生长因子 β1(trans forminggrowthfactor β1,TGF β1)的mRNA表达变化。结果 :在 2 0 μg·L-1rhIL 1β的刺激下 ,(1)正常成熟髁突软骨细胞Ⅱ型胶原和软骨蛋白多糖聚糖体的表达均明显降低 ,胶原酶表达水平变化不明显 ;(2 )在IL 1β的作用下 ,骨关节病软骨细胞对Ⅱ型胶原和胶原酶的表达水平降低 ,对软骨蛋白多糖聚糖体的表达水平无明显影响 ;(3)IL 1β对正常和骨关节病髁突软骨细胞内源性生长因子IGF 1和TGF β1的表达均无明显影响。 结论 :蛋白多糖聚糖体的合成 ,导致髁突软骨病变发生 ,而且能不断干扰骨关节病髁突软骨细胞代谢 ,导致关节软骨基质环境进一步恶化。
Objective: To study the effect of interleukin 1(IL 1β) on the metabolism of osteoarthritic and normal mature condylar chondrocytes in temporomandibular joints, and investigate the role of IL 1β in the pathogenesis of temporomandibular joint osteoarthritis. Methods: The primary generation of osteoarthritic and normal condylar chondrocytes cultured in the monolayer condition was treated with 20 μg·L -1 recombined human interleukin 1β (rhIL 1β), and then collected to be detected with RT PCR method for the cellular metabolism including mRNA expression of type Ⅱ collagen, aggrecan, collagenase, insulin like growth factor 1 (IGF 1), and transforming growth factorβ1(TGFβ1). Results: The normal mature condylar chondrocytes showed the obviously decreased mRNA expression of type Ⅱ collagen and aggrecan after the intervention of exogenous IL 1β, but less influence could be found for the collagenase expression. The osteoarthritic condylar chondrocytes exhibited the decreased mRNA expression of type Ⅱ collagen and collagenase under the effect of IL 1β, while the cellular mRNA expression of aggrecan didn’t change obviously. The intervention of exogenous IL 1β didn't show an obvious influence on the cellular expression of endogenous growth factors such as IGF 1 or TGF β1 for both the normal and osteoarthritic condylar chondrocytes cultured in vitro. Conclusion: IL 1β could not only disturb the expression of cartilage matrix molecules by the normal condylar chondrocytes, which lead to the lesion of condylar cartilage, but also worsen the abnormal cartilage matrix environment within the osteoarthritic condylar cartilage.
出处
《北京大学学报（医学版）》
CAS
CSCD
北大核心
2003年第5期521-524,共4页
Journal of Peking University:Health Sciences
基金
国家自然科学基金 ( 3 9970 795 )资助~~
