摘要
Acute pancreatitis is generally believed to be a disease in which the pancreas is injured by digestive enzymes that it normally produces. Most of the potentially harmful digestive enzymes produced by pancreatic acinar cells are synthesized and secreted as inactive zymogens which are normally activated only upon entry into the duodenum but, during the early stages of acute pancreatitis, those zymogens become prematurely activated within the pancreas and, presumably, that activation occurs within pancreatic acinar cells. The mechanisms responsible for intracellular activation of digestive enzyme zymogens have not been elucidated with certainty but, according to one widely recognized theory （the ＂co-localization hypothesis＂）, digestive enzyme zymogens are activated by lysosomal hydrolases when the two types of enzymes become co-localized within the same intracellular compartment. This review focuses on the evidence supporting the validity of the m-localization hypothesis as an explanation for digestive enzyme activation during the early stages of pancreatitis. The findings, summarized in this review, support the conclusion that co-localization of lysosomal hydrolases with digestive enzyme zymogens plays a critical role in permitting the intracellular activation of digestive enzymes that leads to acinar cell injury and pancreatitis.
尖锐胰腺炎通常被相信是胰被它通常生产的消化酶在伤害的疾病。当是的不活跃的酶原通常仅仅在入口之上激活进十二指肠，但是在尖锐胰腺炎的早阶段期间，那些酶原变得过早地在胰以内并且，大概激活，大多数胰腺的腺泡房间生产的潜在地有害的消化酶被综合并且藏匿那激活发生在胰腺的腺泡房间以内。为消化酶酶原的细胞内部的激活负责的机制没与必然被阐明，但是根据一个广泛地公认的理论(“合作本地化假设”) ，消化酶酶原被 lysosomal 水疗院激活当酶的二种类型在一样的细胞内部的分隔空间以内变得 co 局部性时，放射激光。这评论集中于在胰腺炎的早阶段期间作为对消化酶激活的解释支持合作本地化假设的有效性的证据。调查结果，在这评论总结了，支持 lysosomal 水疗院的合作本地化与消化酶酶原戏放射激光的结论在允许导致腺泡房间损害和胰腺炎的消化酶的细胞内部的激活的一个关键角色。
