Kirkpatrick C J, Mohr W, Haferkamp O
Cell Tissue Res. 1982;224(2):441-8. doi: 10.1007/BF00216885.
Lapine articular chondrocytes were subcultured in the presence or absence of the prostanoid precursors, arachidonic acid or dihomo-gamma-linolenic acid, and the cyclooxygenase inhibitor indomethacin. Lipid storage was studied microscopically using the Sudan black staining method. Control chondrocyte cultures showed a weakly positive staining reaction until confluence was reached, at which point the intra-cytoplasmic lipid content decreased. Both arachidonic acid and dihomo-gamma-linolenic acid at 100 mumol/l caused a marked increase in lipid storage which continued even after confluence was achieved. 1 mumol/l concentrations were indistinguishable from controls, whereas 10 mumol/l concentrations elicited a slight increase in lipid storage compared with controls. The prostaglandin cyclooxygenase inhibitor indomethacin did not affect chondrocyte lipid storage. However, administration of a prostanoid precursor in the presence of indomethacin caused a massive increase in intra-cytoplasmic storage of lipid, eventually leading to cell death. A possible explanation is that indomethacin may alter chondrocyte lipid metabolism in the presence of substrate molecules by rechanneling lipid synthesis away from the prostaglandin pathway to other lipid synthetic pathways.
将兔关节软骨细胞在存在或不存在前列腺素前体、花生四烯酸或二高-γ-亚麻酸以及环氧化酶抑制剂吲哚美辛的情况下进行传代培养。使用苏丹黑染色法在显微镜下研究脂质储存情况。对照软骨细胞培养物在达到汇合之前显示弱阳性染色反应，此时细胞质内脂质含量下降。100μmol/L的花生四烯酸和二高-γ-亚麻酸均导致脂质储存显著增加，即使在达到汇合后仍持续增加。1μmol/L的浓度与对照无差异，而10μmol/L的浓度与对照相比脂质储存略有增加。前列腺素环氧化酶抑制剂吲哚美辛不影响软骨细胞脂质储存。然而，在吲哚美辛存在的情况下给予前列腺素前体导致细胞质内脂质储存大量增加，最终导致细胞死亡。一种可能的解释是，吲哚美辛可能通过将脂质合成从前列腺素途径重新导向其他脂质合成途径，在存在底物分子的情况下改变软骨细胞脂质代谢。
