摘要
使用氨基半乳糖和内毒素建立大鼠急性肝损伤模型。１２ｈ后血清酶及肝血栓素Ａ_２（ＴＸＡ_２）显著升高，肝白三烯Ｃ_４（ＬＴＣ_４）和前列腺素（ＰＧＩ_２）变化不明显。脂氧酶抑制剂能降低血清酶，显著增加肝ＴＸＡ_２生成，对ＬＴＣ_４和ＰＧＩ_２影响不显著。环氧酶抑制剂不能降低血清酶，但使肝ＬＴＣ_４显著升高，ＴＸＡ_２显著降低，对ＰＧＩ_２影响不明显。提示在急性肝损伤时花生四烯酸代谢异常。其代谢产物白三烯和血栓素是导致肝损伤的重要炎症介质。
The changes of the levels of LTC4、PGI2 and TXA2 in the liver tissue of SD rats with GalN/LPS-induced acute liver injury were studied by radioimmunoassay(RIA),12 h after the administration of GalN/LPS,serum AST、ALT increased(P<0.001)and the concentration of TXA2 increased significantly while the content of LTC4 and PGI2 in liver tissue were not obviously changed(P>0.05)and the inflammatory change of liver were observed.The improvement of serum AST and ALT(P<0.05)and histopathological damage was observed after the administration of diethylcarbamazine(DEC),a LTA4 synthesis in hibitor;the liver TXA2 conceration significantly increased while the livels of LTC4 and PGI2 were not obviously changed.Serum ALT and AST levels and histopathology did not change with administration of indomethacin,a cyclooxygenase inhibitor,but the liver LTC4 contents increased and TXA2 reduced significantly,The present study suggests that arachidonic acid metabolism in rats with acute liver injury are significantly abnormal.Leukotrienes and thromboxane are important inflammatory mediators in the liver injury.
出处
《同济医科大学学报》
CSCD
北大核心
1995年第2期112-114,共3页
Acta Universitatis Medicinae Tongji
