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对小鼠进行链脲佐菌素治疗后,照射可预防胰岛退化和高血糖症。

Irradiation protects against pancreatic islet degeneration and hyperglycaemia following streptozotocin treatment of mice.

作者信息

Nedergaard M, Egeberg J, Kromann H

出版信息

Diabetologia. 1983 May;24(5):382-6. doi: 10.1007/BF00251829.

Abstract

Five daily injections of streptozotocin (40 mg/kg) produce islet inflammation, necrosis of pancreatic B cells and hyperglycaemia in the mouse. Anti-pancreatic autoimmunity has been suggested as part of the cause of these events. We have studied the possible effect of total-body irradiation in long-term studies (246 days) and report here that insulitis, islet necrosis and insulin depletion are reduced after irradiation. In parallel the level of hyperglycaemia is reduced. It is concluded that immunological mechanisms are to some extent responsible for the development of streptozotocin-induced diabetes.

摘要

每天注射五次链脲佐菌素(40毫克/千克)会在小鼠体内引发胰岛炎症、胰腺β细胞坏死以及高血糖症。抗胰腺自身免疫被认为是这些事件的部分成因。我们在长期研究(246天)中研究了全身照射的可能影响,并在此报告,照射后胰岛炎、胰岛坏死和胰岛素耗竭有所减轻。同时,高血糖水平也有所降低。结论是免疫机制在一定程度上导致了链脲佐菌素诱导的糖尿病的发展。

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