Andrews J, Halliday G M, Muller H K
Department of Pathology, University of Tasmania, Hobart, Australia.
Clin Exp Immunol. 1991 Jul;85(1):9-13. doi: 10.1111/j.1365-2249.1991.tb05674.x.
Prostaglandins have been implicated in the immune suppression associated with the development of some tumours. Application of the prostaglandin synthetase inhibitor indomethacin, to murine skin prior to treatment with the chemical carcinogens benzo(a)pyrene (BP) or 7,12 dimethylbenz(a)anthracene (DMBA), restored contact sensitivity responses to 2,4-dinitrofluorobenzene in BP- but not DMBA-treated mice. However, indomethacin failed to restore antibody responses in either group of mice. Prolonged treatment with BP or DMBA led to cutaneous tumour formation. Indomethacin was found to delay the onset and reduce the size of tumours in BP- but not DMBA-treated mice. It is proposed that prostaglandin-induced suppression of cellular cutaneous immunity may play a role in BP- but not DMBA-induced cutaneous carcinogenesis.
前列腺素与某些肿瘤发生过程中相关的免疫抑制有关。在用化学致癌物苯并(a)芘(BP)或7,12 - 二甲基苯并(a)蒽(DMBA)处理小鼠皮肤之前,应用前列腺素合成酶抑制剂吲哚美辛,可恢复BP处理而非DMBA处理小鼠对2,4 - 二硝基氟苯的接触敏感性反应。然而,吲哚美辛未能恢复两组小鼠的抗体反应。用BP或DMBA长期处理会导致皮肤肿瘤形成。发现吲哚美辛可延迟BP处理而非DMBA处理小鼠肿瘤的发生并减小肿瘤大小。有人提出,前列腺素诱导的细胞性皮肤免疫抑制可能在BP诱导而非DMBA诱导的皮肤癌发生中起作用。