【摘要】 目的:建立L-精氨酸诱导大鼠暴发性胰腺炎(FAP)肝损伤模型,并探讨FAP肝损伤机制。方法:L-精氨酸分次间隔2h分别于腹腔和皮下注射。末次注射后观察120 h内大鼠死亡率以及6、12、24、48、72和120 h血清淀粉酶、谷丙转氨酶(ALT)、谷草转氨酶(AST)、总胆红素(TBIL)以及门静脉血中肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)含量变化;同时观察各时点胰腺、肝脏病理改变及肝细胞凋亡变化。结果:注射后大鼠120 h内死亡率为53.33%;AST、ALT、TBIL、IL-6、TNF-α于6 h升高,其中AST、TBIL、IL-6于24 h达高峰,ALT、TNF-α于48 h达高峰;胰腺、肝脏病理改变以及肝细胞凋亡均于6 h开始变化,48 h达高峰。结论:大剂量L-精氨酸可诱导大鼠FAP肝损伤模型,TNF-α、IL-6、细胞凋亡可能参与其损伤机制。更多还原

【Abstract】 Objective:To establish the model of fulminant acute pancreatitis(FAP)-associated liver injury induced by L-arginine in rats,and to study the mechanism of hepatic lesion in the model.Methods:Male rats were given intrape-(ritoneal) and subcutaneous injection with L-arginine for 2 times at an interval of 2 hours. After injection,the mortality of rats within 120 hours was observed.At the point of 6,12,24,48,72 and 120 hours,the serum amylase(AMS),alanine aminotraferase(ALT),aspartate aminotrferase(AST),total bilirubin(TBIL),tumor necrosis factor(TNF)-α,interleukin(IL)-6 were tested;the pathological changes of pancreas and liver were observed;and the hepatocytes apoptosis was analyzed.Results:After injection of L-arginine,the mortality of rats within 120 hours was 53.33%; AMS,ALT,AST,TBIL,TNF-α,IL-6 were all increased at 6 hours,and peaked at 24,48,24,24,48,24 hours individually.The pathological alteration of pancreas and liver appeared at 6 hours and peaked at 48 hours.The hepatocytes apoptosis was increased at 6 hours,and reached the top at 48 hours.Conclusion: The administration of L-arginine can induce the model of FAP-associated liver injury in rats,and the mechanism of injury may be related to TNF-α,IL-6 and cells apoptosis.更多还原