Berenbaum F, Thomas G, Poiraudeau S, Béréziat G, Corvol M T, Masliah J
URA CNRS 1283, Faculté de Médecine Saint Antoine, Paris, France.
FEBS Lett. 1994 Feb 28;340(1-2):51-5. doi: 10.1016/0014-5793(94)80171-1.
Interleukin 1 beta was found to stimulate arachidonic acid release, and the synthesis and secretion of type II phospholipase A2 by rabbit articular chondrocytes in vitro. Interleukin 1 beta had no effect on the level of cytosolic phospholipase A2 mRNA. Insulin-like growth factors, which help stabilize the cartilage matrix, reduced the effect of interleukin 1 beta on type II phospholipase A2 activity and mRNA level, and decreased the Interleukin 1 beta-stimulated arachidonic acid release to the basal values. This suggests that type II phospholipase A2 plays a key role in arachidonic acid release from rabbit articular chondrocytes and that insulin-like growth factors counteract the effect of interleukin 1 beta. They may therefore be considered as potential antiinflammatory agents.
研究发现,白细胞介素1β可刺激兔关节软骨细胞在体外释放花生四烯酸,并促进Ⅱ型磷脂酶A2的合成与分泌。白细胞介素1β对胞质磷脂酶A2 mRNA水平无影响。有助于稳定软骨基质的胰岛素样生长因子,可降低白细胞介素1β对Ⅱ型磷脂酶A2活性和mRNA水平的影响,并将白细胞介素1β刺激的花生四烯酸释放量降至基础值。这表明Ⅱ型磷脂酶A2在兔关节软骨细胞释放花生四烯酸过程中起关键作用,且胰岛素样生长因子可抵消白细胞介素1β的作用。因此,它们可被视为潜在的抗炎剂。