Correlation of the biosynthesis of prostaglandin and cyclic AMP in monolayer cultures of rabbit articular chondrocytes.
Correlation of the biosynthesis of prostaglandin and cyclic AMP in monolayer cultures of rabbit articular chondrocytes.
复制标题
兔关节软骨细胞单层培养物中前列腺素和环磷酸腺苷生物合成的相关性。
DOI：
10.1016/0304-4165(82)90051-4
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Papay,RS
中科院分区：
文献类型：
--
作者：
Malemud,CJ;Moskowitz,RW;Papay,RS
我们利用离子载体来测试软骨细胞前列腺素生物合成的刺激是否伴随着这些细胞中环核苷酸水平的增加。前列腺素E2、6-氧代-前列腺素F1α（前列腺素I2的稳定代谢产物）和前列腺素F2α的放射免疫测定表明，在无血清培养基中短期孵育（1-7 min）后，二价阳离子离子载体A23187可刺激每种物质的合成。未检测到血栓素B2的刺激作用。两个单价离子载体，拉沙洛西和莫能菌素未能刺激前列腺素的生物合成后，短期孵育。离子载体A23187刺激的前列腺素生物合成被甲氨蝶呤钠、吲哚美辛和阿司匹林部分抑制，但不被水杨酸钠抑制。离子载体A23187刺激前列腺素的生物合成伴随着环AMP水平增加7.5倍，15分钟后。甲氨蝶呤钠，吲哚美辛和阿司匹林，抑制前列腺素E2的生物合成也降低环AMP水平。外源性前列腺素E_2（1 μg/ml）刺激cAMP的合成，而阿司匹林不抑制。这些结果表明，野牡丹素可以被认为是控制环磷酸腺苷在关节软骨中产生的局部效应之一。
We have utilized ionophores to test whether stimulation of chondrocyte prostaglandin biosynthesis is accompanied by an increase in cyclic nucleotide levels in these cells. Radioimmunoassay of prostaglandin E2, 6-oxo-prostaglandin F1α(the stable metabolite of prostaglandin I2) and prostaglandin F2αshowed that synthesis of each was stimulated by the divalent-cation ionophore, A23187 after short-term incubation (1–7 min) in serum-free medium. No stimulation of thromboxane B2was detected. Two monovalent ionophores, lasalocid and monensin failed to stimulate prostaglandin biosynthesis after short-term incubation. Ionophore A23187-stimulated prostaglandin biosynthesis was variably and partially inhibited by sodium meclofenamate, indomethacin and aspirin, but not by sodium salicylate. Ionophore A23187-stimulated prostaglandin biosynthesis was accompanied by a 7.5-fold increase in cyclic AMP levels after 15 min. Sodium meclofenamate, indomethacin and aspirin which inhibited prostaglandin E2biosynthesis also reduced cyclic AMP levels. Exogenous prostaglandin E2(1 μg/ml) stimulated cyclic AMP biosynthesis, which was not inhibited by aspirin. These results indicated that prostaglandins can be considered as one of the local effectors controlling cyclic AMP production in articular cartilage.