Zhu Hongwei, Yu Xiao, Zhu Shaihong, Li Xia, Lu Ben, Li Zhiqiang, Yu Can
Department of Gastrointestinal and Pancreatic Surgery, Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Department of Endocrinology, Third Xiangya Hospital, Central South University Changsha 410013, Hunan, China.
Int J Clin Exp Pathol. 2015 Sep 1;8(9):11164-70. eCollection 2015.
BACKGROUND & AIMS: Acute pancreatitis is an inflammatory pancreatic disease that carries considerable morbidity and mortality. The pathogenesis of this disease remains poorly understood. We investigated the incidence of autophagy in mice following induction of acute pancreatitis.
Mice were received intraperitoneal injections of L-arginine (200 mg × 2/100 g BW), while controls were administered with saline. Pancreatic tissues were assessed by histology, electron microscopy and western blotting.
Injection of L-arginine resulted in the accumulation of autophagosomes and a relative paucity of autolysosomes. Moreover, the autophagy marker p62 is significantly increased. However, the lysosomal-associated membrane protein-2 (Lamp-2), a protein that is required for the proper fusion of autophagosomes with lysosomes, is decreased in acute pancreatitis. These results suggest that a crucial role for autophagy and Lamp-2 in the pathogenesis of acute pancreatitis.
Our data suggest that the autophagic flux is impaired in acute pancreatitis. The depletion of Lamp-2 may play a role in the pathogenesis of acute pancreatitis.
急性胰腺炎是一种炎症性胰腺疾病，具有较高的发病率和死亡率。该疾病的发病机制仍知之甚少。我们研究了急性胰腺炎诱导后小鼠自噬的发生率。
给小鼠腹腔注射L-精氨酸（200mg×2/100g体重），而对照组给予生理盐水。通过组织学、电子显微镜和蛋白质印迹法评估胰腺组织。
注射L-精氨酸导致自噬体积累，自噬溶酶体相对较少。此外，自噬标志物p62显著增加。然而，溶酶体相关膜蛋白2（Lamp-2），一种自噬体与溶酶体正确融合所需的蛋白质，在急性胰腺炎中减少。这些结果表明自噬和Lamp-2在急性胰腺炎发病机制中起关键作用。
我们的数据表明急性胰腺炎中自噬流受损。Lamp-2的消耗可能在急性胰腺炎的发病机制中起作用。
