L-精氨酸诱导急性胰腺炎小鼠肺损伤的实验研究

Study on Acute Pancreatitis-associated Lung Injury Induced by L-arginine in Mice

目的 建立大剂量 L-精氨酸诱导急性胰腺炎并发肺损伤的小鼠模型 ,并探讨 TNF- α和 ICAM- 1对该模型小鼠肺损伤的作用。方法 给胰腺炎组小鼠腹腔注射 L-精氨酸 (2 g/ kg) ,间隔 1h后同量再注射 1次 ,末次注射后 12 h采用比色法检测小鼠血清淀粉酶活性、放射免疫法测定肺组织 TNF- α的含量 ;2 4 h观察胰腺和肺组织病理变化并采用免疫组织化学染色法检测肺组织 ICAM- 1的蛋白表达。结果 胰腺炎组小鼠血清淀粉酶活性、肺组织 TNF- α的含量、ICAM- 1的表达均高于对照组 ,且差异有显著性 (P<0 .0 5 ) ;胰腺组织和肺组织 HE染色可见典型的炎性改变。结论 大剂量 L-精氨酸可成功诱导急性胰腺炎并发肺损伤的小鼠模型 ,TNF- α和 ICAM- 1可能参与了 L-精氨酸诱导的 AP小鼠的肺损伤机制。

Objective To establish the model of acute pancreatitis (AP)-associated lung injury induced by L-arginine and study the role of TNF-α and ICAM-1 in the model mice. Methods For the establishment of the AP model, the mice were given the first injection (2 g/kg) of L-arginine intraperitoneally and then the second injection in the same way an hour later. At 12 h after the second injection, the animals' serum amylase activities were assayed by colorimetry, and the tumor necrosis factor-alpha (TNF-α) contents of their pancreatic tissue were determined by radioimmunoassay. At 24 h after the second injection, the histopathological changes in the animals' pancreatic and pulmonary tissues were observed. The pulmonary expression and cellular localization of intercellular adhesion molecule-1 (ICAM-1) were characterized by immunohistochemistry. Results The serum amylase activities, TNF-α content and ICAM-1 expression in lung tissue significantly increased in the AP group as compared with those in the control group. Histopathological examinations revealed that the acinar architecture was partially destroyed with necrosis, interstitial edema and inflammatory infiltration at 24 h after the second injection. Conclusion TNF-α and ICAM-1 may play important roles in the mice with acute pancreatitis-associated lung injury.