Correa S G, Bianco I D, Riera C M, Fidelio G D
Departamento de Bioquímica Clínica, CIOUIBIC, Facultad de Ciencias Quimicas, Córdoba, Argentina.
Eur J Pharmacol. 1991 Jun 18;199(1):93-8. doi: 10.1016/0014-2999(91)90640-c.
The influence of total brain gangliosides on acute inflammation was investigated using the rat hind paw edema test. Total gangliosides (10 micrograms/paw) inhibited the edema produced by the injection of bee venom phospholipase A2 (5 micrograms/paw) when the lipids were co-injected or injected 15 min before the phospholipase A2. Sulphatide (10 micrograms/paw) did not inhibit the edema but potentiated it. Gangliosides (40 micrograms/paw) inhibited the edema induced by carrageenin 1% when they were injected 1 h before the agent. However, gangliosides (up to 200 micrograms/paw) failed to inhibit the dextran-induced edema. The edema test was also used to investigate the effect of gangliosides on the production of mediators of inflammation by peritoneal adherent macrophages. Gangliosides inhibited the production of mediators of inflammation only when they were incubated with these cells before the stimulation with phospholipase A2 or carrageenin. Gangliosides did not inhibit the production of mediators of inflammation when arachidonic acid was added to the cells. These results suggest that the anti-inflammatory effect observed with gangliosides is mediated by inhibition at or before endogenous phospholipase activity.
采用大鼠后爪水肿试验研究了全脑神经节苷脂对急性炎症的影响。当共同注射或在注射蜂毒磷脂酶A2(5微克/爪)前15分钟注射神经节苷脂(10微克/爪)时,能抑制由其注射所产生的水肿。硫脂(10微克/爪)不能抑制水肿,反而会使其加重。当在注射1%角叉菜胶前1小时注射神经节苷脂(40微克/爪)时,能抑制由其诱导的水肿。然而,神经节苷脂(高达200微克/爪)未能抑制右旋糖酐诱导的水肿。水肿试验还用于研究神经节苷脂对腹膜黏附巨噬细胞产生炎症介质的影响。神经节苷脂仅在与这些细胞一起在被磷脂酶A2或角叉菜胶刺激前孵育时,才会抑制炎症介质的产生。当向细胞中添加花生四烯酸时,神经节苷脂不会抑制炎症介质的产生。这些结果表明,观察到的神经节苷脂的抗炎作用是通过在内源性磷脂酶活性时或之前的抑制作用介导的。