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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。
Acute liver injury model in rats was established using galactosamine and endotoxin. After 12 hours, the levels of serum enzymes and TXA_2 were significantly increased, while the changes of LTC_4 and PGI_2 were not obvious. Lipoxygenase inhibitors could decrease serum enzymes and significantly increase hepatic TXA 2 production, with no significant effect on LTC_4 and PGI_2. Epoxide enzyme inhibitors can not reduce serum enzymes, but the liver LTC_4 significantly increased, TXA_2 significantly reduced PGI_2 had no significant effect. Suggesting that arachidonic acid metabolism is abnormal in acute liver injury. Its metabolites leukotriene and thromboxane are important inflammatory mediators that cause liver damage.