Mahony S M, Tisdale M J
CRC Experimental Chemotherapy Group, Aston University, Birmingham, UK.
Br J Cancer. 1989 Jul;60(1):51-5. doi: 10.1038/bjc.1989.218.
Administration of either tumour necrosis factor alpha (TNF-alpha) or 16,16-dimethylprostaglandin E2 (PGE2) to female NMRI mice caused a decrease in body weight accompanied by a reduction in both food and water intake and a decrease in carcass water content. A single injection of TNF-alpha caused an enhanced production of PGE2 by spleen cells from treated animals, that was significant within 1 h of treatment, and persisted until at least 6 h. These results suggest that the anorectic effect of TNF-alpha may be mediated by a prostaglandin intermediate. Indomethacin (10 mg kg-1) administered 2 h before TNF-alpha (7.5 x 10(7) U kg-1) caused a significant reduction in the extent of weight loss and inhibited PgE2 production. Administration of indomethacin 0.5-1.5 h before the TNF-alpha had no significant effect on loss of body weight, but still inhibited PgE2 production. Also PgE2 production was still enhanced in response to TNF-alpha administered chronically, despite the inability of prolonged TNF-alpha administration to produce continued loss of body weight. These results suggest that prostaglandins are not involved in the anorectic effect of TNF-alpha.
给雌性NMRI小鼠注射肿瘤坏死因子α（TNF-α）或16,16-二甲基前列腺素E2（PGE2）会导致体重下降，同时伴有食物和水摄入量减少以及胴体含水量降低。单次注射TNF-α会使受治疗动物脾脏细胞产生的PGE2增加，在治疗后1小时内显著增加，并持续至少6小时。这些结果表明，TNF-α的食欲抑制作用可能由前列腺素中间体介导。在注射TNF-α（7.5×10⁷ U/kg）前2小时给予吲哚美辛（10 mg/kg）可显著减轻体重减轻程度并抑制PGE2产生。在注射TNF-α前0.5 - 1.5小时给予吲哚美辛对体重减轻无显著影响，但仍抑制PGE2产生。此外，尽管长期注射TNF-α无法导致体重持续下降，但长期注射TNF-α仍会使PGE2产生增加。这些结果表明，前列腺素不参与TNF-α的食欲抑制作用。
