Ulrich A B, Schmied B M, Matsuzaki H, Lawson T A, Friess H, Andrén-Sandberg A, Büchler M W, Pour P M
UNMC Eppley Cancer Center, University of Nebraska Medical Center, Omaha 68198-6805, USA.
Pancreas. 2001 May;22(4):388-94. doi: 10.1097/00006676-200105000-00009.
The mechanism of tissue alteration in chronic pancreatitis (CP) is still unclear. Different hypotheses have been discussed, including increasing oxidant stress in the acinar cells, often as a result of exposure to xenobiotics. To evaluate the role of oxidative stress in CP, the authors investigated the expression of the drug-metabolizing phase II enzyme, glutathione S-transferase-pi (GST-pi), in the pancreatic tissue of patients with CP and compared it with the healthy pancreatic tissue from age-matched donors. Pancreatic tissue from patients with secondary CP resulting from ductal obstruction by pancreatic cancer (PC) was also examined. The percentage of cells immunoreacting with anti-GST-pi was counted within 15 randomly selected islets in each slide of the three groups. In all specimens, ductal and ductular cells, and in PC, cancer cells, expressed GST-pi in a moderate intensity. Acinar cells did not stain. Various numbers of islet cells in each of the three groups were stained strongly. More islet cells expressed GST-pi in CP (42%) than in healthy pancreatic tissue (16%, p < 0.001) or PC (17%, p < 0.001). Our results imply an important role of islet cells in the metabolism of substances, which are the substrate for GST-pi, and lend support to the hypothesis of oxidative stress as the cause of CP.
慢性胰腺炎（CP）中组织改变的机制仍不清楚。人们已讨论过不同的假说，包括腺泡细胞中氧化应激增加，这通常是接触外源性物质的结果。为了评估氧化应激在CP中的作用，作者研究了CP患者胰腺组织中药物代谢II期酶谷胱甘肽S-转移酶π（GST-π）的表达，并将其与年龄匹配的供体的健康胰腺组织进行比较。还检查了因胰腺癌（PC）导致导管阻塞引起的继发性CP患者的胰腺组织。在三组每张载玻片上随机选择的15个胰岛内，计数与抗GST-π免疫反应的细胞百分比。在所有标本中，导管和小导管细胞，以及在PC中癌细胞，均中等强度表达GST-π。腺泡细胞未染色。三组中每组都有不同数量的胰岛细胞被强烈染色。CP中表达GST-π的胰岛细胞（42%）多于健康胰腺组织（16%，p<0.001）或PC（17%，p<0.001）。我们的结果表明胰岛细胞在作为GST-π底物的物质代谢中起重要作用，并支持氧化应激是CP病因的假说。
