Hyperlipidemia intensifies cerulein-induced acute pancreatitis associated with activation of protein kinase C in rats

AIM： To investigate the effects of hyperlipidemia on acute pancreatitis （AP） and the possible mechanisms. METHODS： Rat models of hyperlipidemia and AP were established by Triton WR1339 and cerulein respectively. Human albumin was used to treat AP complicated by hyperlipidemia. In each group, we compared the histological score, volume of ascites, ratio of pancreatic wet/dry weight, serum amylase （AMY） and pancreatic acinar cell apoptosis. The level of protein kinase C （PKC） membrane translocation in pancreatic tissue was detected by Western blot.RESULTS： In the hyperlipidemia model established by Triton WR1339, triglyceride （TG） increased remarkably and reached its peak 6 h after injection, and most rats developed mild acute pancreatitis. Histological score, volume of ascites, ratio of wet/dry weight and serum AMY in AP animals with hyperlipidemia were obviously higher than those in AP animals （P 〈 0.05） and decreased after albumin therapy but not significantly （P 〉 0.05）. Apoptotic cells detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL） increased in AP animals with hyperlipidemia and did not change distinctly after albumin therapy. PKC membrane translocation level increased in AP animals with hyperlipidemia and decreased remarkably after albumin therapy （P 〈 0.05）.CONCLUSION： Hyperlipidemia may induce AP or intensify pancreatic injury. Albumin therapy can not alleviate pancreatic lesion effectively. PKC activation may be one mechanism by which AP is intensified by hyperlipidemia.

瞄准：在尖锐胰腺炎(AP ) 和可能的机制上调查 hyperlipidemia 的效果。方法：hyperlipidemia 和 AP 的老鼠模型被三重氢核 WR1339 和 cerulein 分别地建立。人的白朊被用来对待由 hyperlipidemia 复杂的 AP。在每个组，我们比较了组织学的分数，腹水的体积，胰腺的湿 / 干燥的重量的比率，浆液淀粉酶(AMY ) 和胰腺的腺泡房间 apoptosis。在胰腺的织物的蛋白质激酶 C (PKC ) 膜易位的水平被西方的污点检测。结果：在三重氢核 WR1339 建立的 hyperlipidemia 模型，甘油三酸酯(TG ) 显著地增加了并且到达了它的山峰在注射以后的 6 h，和大多数老鼠开发了温和尖锐胰腺炎。组织学的分数，腹水的体积，湿 / 干燥的重量的比率和在有 hyperlipidemia 的 AP 动物的浆液 AMY 显然比在 AP 动物的那些高(P < 0.05 ) 并且在白朊治疗以后然而并非显著地减少了(P > 0.05 ) 。Apoptotic 房间由标记的调停 transferase 的 dUTP-biotin 刻痕结束(TUNEL ) 与 hyperlipidemia 在 AP 动物增加了的终端 deoxynucleotidyl 检测了并且没在白朊治疗以后清楚地变化。与 hyperlipidemia 在 AP 动物增加并且在白朊治疗以后显著地减少了的 PKC 膜易位水平(P < 0.05 ) 。结论：Hyperlipidemia 可以导致 AP 或加强胰腺的损害。白朊治疗不能有效地减轻胰腺的损害。PKC 激活可以是 AP 被 hyperlipidemia 被加强的一机制。