Abstract
Experimental liver injury models were produced by the injection of anti-basic liver protein (BLP) antibody into DBA/2 mice, by the injection of bacterial LPS into Corynebacterium parvum-pretreated ddY mice, and by the injection of CCl4 into ddY mice. In all models, extensive liver cell damage was estimated by the elevation of glutamate transaminase (GOT and GPT) activity and confirmed by significant histopathological changes of liver. Moreover, significant elevation of TxB2 in the liver was observed in all models.
Administration of OKY-046, a selective TxA2 synthetase inhibitor, ONO-3708, TxA2 receptor antagonist, and indomethacin, cyclooxygenase inhibitor, suppressed the elevation of GOT and GPT levels and histopathological changes in almost liver injury models. In addition, when U-46619, a stable TxA2 mimetic compound, was injected into mice, clear elevation of GOT and GPT was observed. These evidences suggest that TxA2 play an important role for the onset of liver injury disease in mice.
