论文部分内容阅读
目的探讨1型糖尿病(T1DM)小鼠胰岛表达CD68、CD22的改变,血清白介素-12(IL-12)、白介素-4(IL-4)水平的变化及可能的机制。方法正常雄性C57BL/6J小鼠104只,随机分为正常对照组、盐水对照组及实验组。小剂量多次注射链脲佐菌素(MLD-STZ)建立1型糖尿病小鼠模型,分别于第3、7、10、14、21、28天测空腹血糖,取胰尾组织及血清,通过免疫组化SABC法、酶联免疫吸附法(ELISA)及形态计量法进行研究。结果与正常及盐水对照组相比较,实验组小鼠胰岛数目减少,胰岛面积减小。实验组小鼠胰岛CD68阳性细胞的面数密度(NA)于第3天起明显高于正常对照组和盐水对照组(P<0.01),但第10天的NA在实验组相对较低。实验组胰岛CD22阳性细胞的NA值于第3天即高于正常对照组和盐水对照组(P<0.01),至第7天最高。血清ELISA结果显示,实验组小鼠血清IL-12水平自第7天开始增高(P<0.05);而血清IL-4水平与正常及盐水对照组相比有所降低,差异有统计学意义(P<0.05)。结论 CD68及CD22阳性细胞在T1DM早期即浸润胰岛,有可能通过抗原递呈等作用促进了T1DM的发生。实验组小鼠血清IL-12增高,IL-4减少,提示Th1/Th2细胞失衡,推测是引发T1DM的重要因素之一。
Objective To investigate the changes of CD68 and CD22 expression, the levels of interleukin-12 (IL-12) and interleukin-4 (IL-4) in islet cells of type 1 diabetic mice and their possible mechanisms. Methods A total of 104 normal male C57BL / 6J mice were randomly divided into normal control group, saline control group and experimental group. Small doses of multiple injections of streptozotocin (MLD-STZ) to establish a type 1 diabetic mouse model, respectively, on the 3rd, 7th, 10th, 14th, 21st and 28th days of fasting blood glucose, tail and tail tissue and serum, Immunohistochemical SABC method, enzyme-linked immunosorbent assay (ELISA) and morphometry were studied. Results Compared with the normal saline control group, the number of islets in experimental mice decreased and the islet area decreased. The number density (NA) of CD68 positive cells in the experimental group was significantly higher than that in the normal control group and saline control group on the third day (P <0.01), but the NA on the tenth day was relatively lower in the experimental group. The NA value of CD22 positive cells in experimental group was higher than that in normal control group and saline control group on the third day (P <0.01), and reached the highest on the seventh day. Serum ELISA results showed that serum IL-12 level in the experimental group increased from the 7th day (P <0.05), while serum IL-4 level was lower than that in the normal and saline control groups (P <0.05) P <0.05). Conclusion CD68 and CD22 positive cells infiltrated the islets in the early stage of T1DM, which may promote the occurrence of T1DM through the action of antigen presentation. Experimental group mice serum IL-12 increased, IL-4 decreased, suggesting that Th1 / Th2 cells imbalance, presumably is one of the important factors triggering T1DM.