Morphological, immunocytochemical and biochemical studies in human osteoarthritic chondrocytes exposed to IL-1b and cyclical hydrostatic pressure

Clinical and Experimental Rheumatology

G. Collodel¹  E. Moretti¹  G. Scapigliati¹  A. Fioravanti¹  M. Galeazzi¹  R. Cervone¹ 

关键词: Chondrocytes;    hydrostatic cyclical pressure;    interleukin-1β;    nitric oxide;    osteoarthritis.;   

DOI  :  

学科分类：医学（综合）

来源: Pacini Editore SpA

【 摘 要 】

OBJECTIVES:To investigate the in vitro effects of cyclic hydrostatic pressure (HP), of a magnitude and frequency close to those that presumably exist in articular cartilage, on human osteoarthritic chondrocytes cultivated for 48 hrs in the presence or absence of interleukin-1Β (IL-1Β).METHODS:Pressurization cycles in the form of sinusoidal waves (minimum pressure 1 MPa, maximum pressure 5 MPa) at a frequency of 0.25 Hz for 3h were assessed on cultured chondrocytes obtained from the femoral heads of osteoarthritic patients. Under these conditions, we evaluated proteoglycan (PG) levels and nitrites production in the culture medium by the immunoenzymatic method and examined the morphology of chondrocytes by transmission electron microscopy (TEM). Moreover, immunocytochemical investigations were performed to localize inducible nitric oxide synthase (iNOS).RESULTS:The presence of IL-1Β led to a very significant decrease in PG levels and to an increase in NO production. When the chondrocytes were cultured in the presence of HP, a statistically significant restoration of PG levels was observed, but pressurization did not significantly increase the PG levels in cells damaged by IL-1Β. After pressurization, there was a slight decrease in the concentration of NO under basal conditions and a statistically significant decrease in the IL-1Β induced release of NO. The results concerning metabolic production were further confirmed by the morphological findings obtained by TEM and immunocytochemical studies.CONCLUSIONS:This study confirms the protective role of HP which stimulates PG production and counteracts IL-1Β induced NO release. These data are supported by morphological and immunocytochemical findings.

【 授权许可】

Unknown