Bakhle Y S
Eur J Pharmacol. 1980 Dec 19;68(4):493-6. doi: 10.1016/0014-2999(80)90425-2.
Sulphasalazine 10(-4M) inhibited PGE2 inactivation in isolated perfused lungs from guinea pig, rat and man and, in guinea pig and rat lungs, inhibited 16,16-dimethyl PGE2 inactivation and accelerated efflux of radioactivity following injection of [14C]PGE2. In rat and human, but not in guinea-pig lung, sulphasalazine inhibited activation of exogenous arachidonate to PG-like substances. Thus sulphasalazine inhibited PG inactivation by inhibiting PG uptake; there was a marked species difference in its effects on arachidonate activation.
柳氮磺胺吡啶10(-4M)抑制豚鼠、大鼠和人离体灌注肺中PGE2的失活,并且在豚鼠和大鼠肺中,抑制16,16 - 二甲基PGE2的失活,并在注射[14C]PGE2后加速放射性流出。在大鼠和人的肺中,而不是豚鼠肺中,柳氮磺胺吡啶抑制外源性花生四烯酸激活为PG样物质。因此,柳氮磺胺吡啶通过抑制PG摄取来抑制PG失活;其对花生四烯酸激活的影响存在明显的种属差异。