摘要
目的 :探讨新生期胰岛素干预对NOD鼠 1型糖尿病的预防作用及其机制。方法 :采用NOD鼠作动物模型 ,新生期胰岛素干预后检测血糖、尿糖及糖尿病发病率 ,HE染色观察胰岛炎 ,用RT PCR法检测胰腺干扰素γ(IFN γ)、肿瘤坏死因子α(TNF α)、白介素 10 (IL 10 ) ,免疫组化检测胰腺胰岛细胞Bcl 2和Bax表达。结果 :新生期胰岛素干预组糖尿病发病率为31 6 % ,明显低于对照组 (72 2 % ) (P <0 0 1) ,且胰岛炎严重程度也明显减轻 (P <0 0 1)。胰腺TNF α、IFN γmRNA的表达较对照组显著降低 (P <0 0 1) ;IL 10mRNA的表达增强 (P <0 0 1)。胰腺胰岛Bcl 2表达明显增强 ,而Bax表达较对照组明显减弱。结论 :新生期胰岛素干预可以预防NOD鼠糖尿病的发生 ,其机制可能与纠正Th1型细胞因子与Th2型细胞因子比例失衡 ,进而上调胰岛β细胞Bcl
Objective:To detect the effect of administration of insulin on type 1 diabetes and its possible machines. Methods:64 female NOD mice were randomly divided into 2 groups. The mice were administered respectively insulin (0 25 U) in 0 1 ml PBS in treated group and PBS 0 1 ml in control by intraperitoneal injection within 24 h as neonates. The mice were reimmunized at 2,3,4 and 9 th week. 12 mice of each group were killed at 15th week. Pancreases were removed to examine insulitis scores through HE straining. And expression of Bcl 2 and Bax on islet cells were detected by immunohistochemical straining. Levels of cytokines mRNA of pancreases were measured by RT PCR. 20 mice were used to evaluate incidence of diabetes. The mice were considered diabetes when urine was positive, and blood glucose was consistently >13 2 mmol/L. Results:The incidence of diabetes in the treated group was 31 6% which was obviously less than 72 2% in control group ( P <0 01), and the degree of insulitis in the treated group was also less than in the control group. IFN γ and TNF α mRNA expression were significantly downregulated, while IL 10mRNA increased markedly in pancreas of treated group (P <0 01). The expression of Bcl 2 on islet cells was stronger in treated group ( P <0 05), while the Bax weaker in treated group (P <0 05). Conclusion:Insulin administered in mice as neonates can prevent NOD mice from developing type 1 diabetes, probably through regulating Th1/Th2 imbalance, and then increasing the expression of Bcl 2 and decreasing the expression of Bax on islet.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2004年第7期490-493,共4页
Chinese Journal of Immunology
基金
山西省自然科学基金资助项目 (2 0 0 2 3 9)
