EFFECTS OF 3 AVOCADO SOYBEAN UNSAPONIFIABLE MIXTURES ON METALLOPROTEINASES, CYTOKINES AND PROSTAGLANDIN E-2 PRODUCTION BY HUMAN ARTICULAR CHONDROCYTES/

Citation
Ye. Henrotin et al., EFFECTS OF 3 AVOCADO SOYBEAN UNSAPONIFIABLE MIXTURES ON METALLOPROTEINASES, CYTOKINES AND PROSTAGLANDIN E-2 PRODUCTION BY HUMAN ARTICULAR CHONDROCYTES/, Clinical rheumatology, 17(1), 1998, pp. 31-39
Citations number
42
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
07703198
Volume
17
Issue
1
Year of publication
1998
Pages
31 - 39
Database
ISI
SICI code
0770-3198(1998)17:1<31:EO3ASU>2.0.ZU;2-A
Abstract
The in-vitro effects of avocado and soybean unsaponifiable residues on neutral metalloproteinase activity, cytokines and prostaglandin E-2 ( PGE(2)) production by human articular chondrocytes were investigated. Avocado and soybean unsaponifiable residues were mixed in three ratios : 1:2 (A1S2), 2:1 (A2S1) or 1:1 (A2S2). Freshly isolated human chondro cytes were cultured for 72 h in the absence or presence of interleukin -1 beta (IL-1 beta) (17 ng/ml), with or without unsaponifiable residue mixtures at a concentration of 10 mu g/ml. A/S unsaponifiable residue s were also tested separately at concentrations of 3.3, 6.6 and 10 mu g/ml. All A/S unsaponifiable mixtures reduced the spontaneous producti on of stromelysin, interleukin-6 (IL-6), interleukin-8 (IL-8) and pros taglandin E-2 (PGE(2)) by chrondrocytes. At concentrations of 3.3 and 6.6 mu g/ml, A/S residues, tested separately, were potent inhibitors o f the production of IL-8 and PGE(2). Nevertheless, only avocado residu e inhibited IL-6 production at these concentrations. AIS unsaponifiabl e mixtures had a more pronounced inhibitory effect on cytokine product ion than avocado or soybean residues added alone. As anticipated, IL-1 beta induced a marked release of collagenase, stromelysin, IL-6, IL-8 and PGE(2). A/S unsaponifiable mixtures partially reversed the IL-1 e ffects on chrondrocytes. These findings suggest a potential role for A /S unsaponifiable extracts in mitigating the deleterious effects of IL -1 beta on cartilage.