免疫机制参与生长抑素对链佐霉素诱发的小鼠胰岛β细胞损伤的保护

IMMUNOLOGICAL MECHANISM INVOLVED IN THE PROTECTIVE ACTION OF SOMATOSTATIN AGAINST THE DAMAGE INDUCED BY STREPTOZOTOCIN ON PANCREATIC ISLETS CELLS IN MICE

连续多次小剂量注射链佐霉素(STZ)后,小鼠产生严重糖尿病,同时出现胸腺萎缩,脾内巨噬细胞增加,脾小结减少,血中淋巴细胞百分数明显下降,胰岛局部淋巴细胞浸润。在每次给STZ前10min注射生长抑素,小鼠血糖及血清胰岛素基本正常,STZ对全身主要免疫器官的破坏程度均减轻,胰岛局部淋巴细胞浸润消失。实验结果提示,免疫机制在一定程度上参与了生长抑素对胰岛β细胞的保护。

Multiple injections of streptozotocin (STZ) not only damaged the islet β cells but also causedatrophy of thymus, increased macrophage in spleen, decreased lymphocytes in blood, and causedlymphocytes infiltration in islets. All the above observations could be partially prevented whensomatostatin (10μg/kg) was given subcutaneously 10 minutes prior to each STZ injection. Thedifferences between STZ damage group and somatostatin protective group were significant. Theseresults suggest that immunological mechanism might be involved to some degree in the protectiveaction of somatostatin against the damage of islets by STZ in mice.