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应用肝大部切除（２／３ＰＨ）后再生肝模型，观察大鼠再生肝内ＰＧＥ２含量变化与再生肝抗四氯化碳损伤的关系。结果：肝切后残余肝内ＰＧＥ２含量有明显变化。２／３ＰＨ后６ｈ，残余肝内ＰＧＥ２含量明显升高，１２ｈ达到高峰，较正常及假手术大鼠差异显著，２４ｈ后ＰＧＥ２含量逐渐恢复至正常水平。肝切后连续给予阿斯匹林（５０ｍｇ／ｋｇＢＷｉｐ）以阻断体内ＰＧ的合成，７２ｈ后用ＣＣｌ４（５０％，与豆油混合）染毒大鼠，阿斯匹林处理组较对照组大鼠死亡率显著增加，血清丙氨酸氨基转移酶显著升高，肝组织损伤程度加重。此外，阿斯匹林处理组大鼠肝湿重／体重比较对照组也显著降低。提示：ＰＧＥ２参与大鼠再生肝抗ＣＣｌ４损伤，其机制很可能是ＰＧ促进残余肝的再生，减轻肝细胞内转氨酶的漏出，维持细胞膜的稳定性。
The liver model was regenerated by subtotal hepatectomy (2 / 3PH) to observe the relationship between the changes of PGE2 content in the regenerated liver and the anti-carbon tetrachloride damage in regenerative liver. Results: There was a significant change of PGE2 content in the residual liver after liver resection. After 2 / 3PH for 6h, the content of PGE2 in the remnant liver increased significantly and peaked at 12h, which was significantly different from that in normal and sham-operated rats. After 24h, the content of PGE2 gradually returned to its normal level. After hepatectomy, aspirin (50mg / kg B Wip) was continuously administered to block the synthesis of PG in vivo. After 72h, rats were treated with CCl4 (50% mixed with soybean oil), and aspirin-treated rats The mortality of rats in the control group increased significantly, serum alanine aminotransferase increased significantly, and liver injury increased. In addition, liver wet weight / body weight in aspirin-treated rats was also significantly reduced compared with the control group. It is suggested that PGE2 is involved in the anti-CCl4 injury in rat regenerative liver. The mechanism is probably that PG promotes the regeneration of residual liver, relieves the leakage of transaminase in liver cells and maintains the stability of cell membrane.