【摘要】 目的　通过检测bcl 2、bax在脾脏、胰腺的表达旨在探讨IV型磷酸二酯酶抑制剂咯利普兰 (rolipram)对NOD小鼠的免疫干预机制。方法　将 60只体重相近的 4周龄雌性NOD小鼠随机分为干预、对照两组 ,每组 3 0只。干预组腹腔注射咯利普兰 (8mg/kg) ,每日两次 ;对照组注射等次等量的PBS。两组小鼠均于实验第 1和第 14天各注射 1次环磷酰氨 (2 0 0mg/kg)以加速糖尿病的进程。实验第 3 0天处死 ,HE染色观察胰岛炎 ;免疫组化检测bcl 2 ,bax在胰岛、脾脏的表达。结果　咯利普兰处理组在胰岛过表达bcl 2基因 (P <0 .0 1) ,而在脾脏过表达bax基因 (P <0 .0 1) ;PBS对照组与咯利普兰处理组相反。结论　咯利普兰在胰腺组织能促进bcl 2的表达以抑制胰岛 β细胞的凋亡 ;而在淋巴系统却能促进bax的表达以加速T淋巴细胞的凋亡从而减轻自身免疫反应更多还原

【Abstract】 Objective To investigate the immune effect of rolipram on nonobese diabetic mice. Methods Sixty female 4-week NOD mice were randomly divided into 2 equal groups. Group 1 received the intraperitoneal injection of rolipram (8 mg/kg) twice every day. Group 2 received the intraperitoneal injection of PBS(equal quantity and times). Two groups’ mice were administered cyclophosphamide(200 mg/kg) to accelerate the process of diabetes on the 1st day and the 14th day respectively. All mice were killed at day 30. When the experiment was finished, the degree of insulitis and the expression of bcl-2 and bax were detected with immunohistochemical technique. Results After intraperitoneal injection of rolipram to NOD mice, the insulitis score and the severity of insulitis in treatment group was lower than those in control group (P<0.01). The expression of bcl-2 in treatment group was higher than that in control group in pancreases (P<0.01). The expression of bax was higher in treatment group than in control group in spleen (P<0.01). Conclusion These results show that rolipram can prevent NOD mice from developing into type 1 diabetes.更多还原