Eizirik D L, Sandler S
Department of Medical Cell Biology, Uppsala University, Sweden.
Pharmacol Toxicol. 1988 Nov;63(5):396-9. doi: 10.1111/j.1600-0773.1988.tb00975.x.
The molecular mechanisms behind the functional responses of the beta-cells after cytotoxic damage are still largely unknown. The aim of this study was to investigate to what extent the islet beta-cells are capable of repairing cellular injuries after acute treatment with increasing doses of alloxan. Isolated mouse pancreatic islets were exposed for 30 min. at 37 degrees to alloxan (1.0, 1.5 and 2.0 mM) or vehicle alone (controls). Immediately after alloxan exposure the islet glucose-stimulated insulin release was severely decreased, and there were morphological evidences of partial necrosis of the islets. After further six days in culture, there was a marked decrease in islet number in the groups of islets treated with 1.5 or 2.0 mM alloxan. However, the DNA and insulin contents of the remaining islets were similar to the values observed in cultured control islets. Furthermore, the insulin secretory response to glucose and the light microscopical appearance of these islets were largely restored on day 6. It is concluded that beta-cells surviving after an injury induced by alloxan may recover their functional capacity after an initial period of inhibited function.
细胞毒性损伤后β细胞功能反应背后的分子机制在很大程度上仍然未知。本研究的目的是调查胰岛β细胞在用递增剂量的四氧嘧啶急性处理后修复细胞损伤的能力。将分离的小鼠胰岛在37℃下暴露于四氧嘧啶（1.0、1.5和2.0 mM）或单独的载体（对照）30分钟。四氧嘧啶暴露后，胰岛葡萄糖刺激的胰岛素释放立即严重减少，并且有胰岛部分坏死的形态学证据。在进一步培养六天后，用1.5或2.0 mM四氧嘧啶处理的胰岛组中胰岛数量显著减少。然而，剩余胰岛的DNA和胰岛素含量与培养的对照胰岛中观察到的值相似。此外，在第6天，这些胰岛对葡萄糖的胰岛素分泌反应和光学显微镜外观在很大程度上恢复。得出的结论是，四氧嘧啶诱导损伤后存活的β细胞在功能受到初始抑制期后可能恢复其功能能力。
