Wellmann K F, Volk B W
Diabetologia. 1977 Aug;13(4):331-7. doi: 10.1007/BF01223275.
Cortisone pretreatment considerably enhances the mortality of young, male, streptozotocin-injected Holtzman rats. In those that survive, cortisone pretreatment decreases the ensuing hyperglycaemia, extends the period during which streptozotocin-induced B cell damage can be observed from less than two to as much as four to seven days and permits the persistence of poorly granulated B cells in such animals. These effects are at least partially attributable to a cortisone-induced augmentation of the total B cell mass. Compared with the high degree of protection against alloxan-induced damage afforded the pancreatic B cells of cortisone-pretreated rabbits, the protective effect of cortisone against B cell destruction in streptozotocin-injected rats is thus much more limited in scope. Species differences as well as differing pathogenetic mechanisms may account for these results.
可的松预处理会显著提高年轻雄性经链脲佐菌素注射的霍尔兹曼大鼠的死亡率。在存活的大鼠中,可的松预处理可降低随后出现的高血糖症,将可观察到链脲佐菌素诱导的B细胞损伤的时间段从不到两天延长至多达四到七天,并使此类动物中颗粒较少的B细胞持续存在。这些作用至少部分归因于可的松诱导的总B细胞量增加。与可的松预处理的兔子的胰腺B细胞对四氧嘧啶诱导的损伤具有高度保护作用相比,可的松对经链脲佐菌素注射的大鼠B细胞破坏的保护作用范围要有限得多。物种差异以及不同的发病机制可能是这些结果的原因。