高脂血症对大鼠急性胰腺炎影响及白蛋白的干预效应

Effects of hyperlipaemia on acute pancreatitis and the intervening effect of albumin therapy in rats

目的探讨高脂血症对急性胰腺炎的影响及白蛋白的干预效应。方法分别用Triton WR1339、Cerulein制作大鼠高脂血症和急性胰腺炎(acute pancreatitis,AP)模型,同时应用两者制作伴有高脂血症的AP模型,应用白蛋白治疗伴有高脂血症的AP,比较各组胰腺病理损害评分、腹水量、胰腺湿/干比、血清淀粉酶和胰腺组织的凋亡;Western blot检测胰腺组织PKC的膜转位。结果Triton WR1339诱导大鼠高脂血症以TG升高为主,6h达高峰,升高达20倍,使部分大鼠出现轻型急性胰腺炎。伴有高脂血症的AP组病理评分、腹水量、胰腺湿/干比和血清淀粉酶较Cerulein胰腺炎组均显著升高(P<0.05),白蛋白治疗后均有所下降,但差异无统计学意义。TUNEL法测得伴有高脂血症的AP腺泡出现凋亡数量最多,白蛋白治疗后无明显的变化。合并高脂血症胰腺炎组PKC膜转位比例最高,白蛋白治疗后显著下降(P<0.05)。结论高脂血症可以诱导AP或加重AP的胰腺损伤,白蛋白治疗不能减轻胰腺的病变。PKC的活化可能是高脂血症加重急性胰腺炎的机制之一。

Objective To investigate the effects of hyperlipaemia on acute pancreatitis （AP） and the intervening effect of albumin. Methods Hyperlipaemia and AP model were established with Triton WR1339 and Cerulein respectively. AP with hyperlipaemia model was prepared by both Triton WR1339 and cerulein simultaneously. Human albumin was used to treat the AP accompanied with hyperlipaemia. In each group, the histological score, volume of ascites, ratio of pancreatic wet/dry weigh, serum amylase and pancreatic acinar cell apoptosis in each group were compared. The level of protein kinase C （PKC） membrane translocation in pancreatic tissue was detected by Western blot. Results In the hyperlipaemia model established with Triton WR1339, triglyceride was increased remarkably and reached the peak about 20 times than that of the control group at 6 hour after injection, and mild acute pancreatitis appeared in most rats. Histological score, volume of ascites, ratio of wet/dry weigh and serum amylase in AP with hyperlipaemia group were obviously higher than that of cerulein AP group （P〈0.05） and decreased after albumin therapy, but there was no significant difference （P〉0.05）. Apoptosis cells detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL） increased in AP with hyperlipaemia group and did not change distinctly after albumin therapy. PKC membrane translocation level enhanced mostly in AP with hyperlipaemia group and decreased remarkably after albmin （P〈0.05）. Conclusion Hyperlipaemia may induce AP or intensify pancreatic injury of AP. Albumin therapy can not alleviate pancreatic lesion effectively. PKC activation may be one of the mechanism of AP acute intensified by hyperlipaemia.