Ohnishi H, Ito C, Suzuki K, Kitamura Y, Shimora M, Saito A, Itoh R
Nihon Yakurigaku Zasshi. 1982 Jun;79(6):561-9.
Effects of protizinic acid (PRT) on prostaglandins (PG) and the production of oxygen radicals were compared with those of other non-steroidal anti-inflammatory agents. Oral administration of 30 mg/kg of PRT, indomethacin (IM), or ibuprofen (IB) significantly inhibited arachidonic acid-induced erythema in guinea pigs. Although 30 mg/kg of PRT significantly inhibited PGE2-induced erythema, IM and IB did not significantly inhibit it. PRT inhibited phospholipase A2 (PLA2) activity, and the IC50 value was 2.1 X 10-4 M. On the other hand, IM and IB exerted no effect on the PLA2 activity at 3 X 10-4 M. These results suggest that PRT possesses a broader pharmacological activity on the PG system than IM and IB. As for effects on the production of oxygen radicals, in order of relative inhibitory potency was PRT greater than metiazinic acid (MA) = IM greater than IB = phenylbutazone (PB) in the xanthine oxidase assay, PB great than IM greater than PRT greater than MA = IB in the rabbit neutrophil myeloperoxidase assay, and IM greater than PB greater than PRT greater than MA greater than IB in the guinea pig macrophage assay. In the rabbit neutrophil and aggregated IgG-bound micropore filter assay, the order was PRT greater than MA greater than PB greater than IM = IB. Thus, the inhibitory effects of PRT was verified in all experiments on the production of oxygen radicals in contrast to IB. In particular, it could be especially meaningful that PRT showed the most potent activity in the aggregated IgG-bound micropore filter assay which has been reported to be a good model for studying the pathogenesis of inflammatory diseases believed to be caused by immune complexes.
将原儿茶酸（PRT）对前列腺素（PG）和氧自由基产生的影响与其他非甾体抗炎药进行了比较。口服30mg/kg的PRT、吲哚美辛（IM）或布洛芬（IB）可显著抑制花生四烯酸诱导的豚鼠红斑。虽然30mg/kg的PRT可显著抑制PGE2诱导的红斑，但IM和IB并未显著抑制。PRT抑制磷脂酶A2（PLA2）活性，IC50值为2.1×10-4M。另一方面，IM和IB在3×10-4M时对PLA2活性无影响。这些结果表明，PRT在PG系统上具有比IM和IB更广泛的药理活性。至于对氧自由基产生的影响，在黄嘌呤氧化酶试验中，按相对抑制效力顺序为PRT大于甲硫氮卓酸（MA）=IM大于IB=保泰松（PB）；在兔中性粒细胞髓过氧化物酶试验中，PB大于IM大于PRT大于MA=IB；在豚鼠巨噬细胞试验中，IM大于PB大于PRT大于MA大于IB。在兔中性粒细胞和聚集IgG结合微孔滤膜试验中，顺序为PRT大于MA大于PB大于IM=IB。因此，与IB相比，PRT在所有氧自由基产生实验中的抑制作用均得到验证。特别是，PRT在聚集IgG结合微孔滤膜试验中表现出最强的活性，这一点可能尤其有意义，因为该试验已被报道是研究认为由免疫复合物引起的炎症性疾病发病机制的良好模型。
