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低剂量链脲佐菌素诱导的小鼠糖尿病免疫调节研究表明,胰岛炎并非B细胞破坏的必要条件。

Immunomodulation of low dose streptozocin diabetes in mice reveals that insulitis is not obligatory for B cell destruction.

作者信息

Papaccio G, Chieffi Baccari G, Esposito V

机构信息

Institute of Anatomy, School of Medicine I, University of Naples, Italy.

出版信息

J Anat. 1992 Dec;181 ( Pt 3)(Pt 3):403-7.

Abstract

Twenty male C57Bl/J mice were injected with 50 microliters complete Freund's adjuvant (CFA) 1 wk before and 1 wk after induction of diabetes with 45 mg streptozocin (STZ)/kg body weight i.p. over 5 d. CFA administration prevented islet infiltration. Inflammatory cells were not seen within any of the islets observed. However, islet B cell destruction still occurred. These cells showed evidence of considerable damage, containing swollen mitochondria, contracted nuclei and areas of vacuolation and degranulation. Inflammation is therefore not obligatory for the development of low dose STZ induced diabetes.

摘要

20只雄性C57Bl/J小鼠在腹腔注射45 mg链脲佐菌素(STZ)/kg体重诱导糖尿病前1周和诱导后1周,分别注射50微升完全弗氏佐剂(CFA),持续5天。给予CFA可防止胰岛浸润。在所观察的任何胰岛内均未见到炎性细胞。然而,胰岛B细胞破坏仍会发生。这些细胞显示出明显受损的迹象,包括线粒体肿胀、细胞核收缩以及空泡化和脱颗粒区域。因此,炎症并非低剂量STZ诱导糖尿病发生所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c775/1259692/6c10d3175a74/janat00149-0013-a.jpg

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