摘要
目的 探讨细粒棘球蚴抗原B对小鼠1型糖尿病发病的早期影响及其机制.方法 30只BALB/c小鼠随机分组:细粒棘球蚴抗原B+糖尿病组(A组);生理盐水+糖尿病组(B组);糖尿病组(C组);A组给予细粒棘球蚴抗原B,B组给予生理盐水,随后A、B、C组均给予小剂量链脲佐菌素诱导1型糖尿病.观察血糖变化,留取标本进行细胞因子等指标测定.结果 在糖尿病成模后3周,A组<40%的胰岛可见淋巴细胞浸润,B组和C组有80%的胰岛见淋巴细胞浸润,差异有统计学意义(A组、B组和C组的平均Ridit值分别为:0.423、0.519、0.561,P<0.05);糖尿病模型建立3周末,A组小鼠血清白细胞介素-4(IL-4)水平高于B组和C组[(71.6±12.4) ng/ml比(12.6±5.6) ng/ml和(14.2-7.2) ng/ml,P<0.05],A组小鼠血清γ-干扰素(IFN-γ)水平低于B组和C组[(276.1 ±41.7) ng/ml比(352.2±52.2)ng/ml和(358.1 ±53.4) ng/ml,P<0.05]. 结论 细粒棘球蚴抗原B对小鼠1型糖尿病早期胰岛细胞的自身免疫损害具有拮抗作用,其机制可能与Th1/Th2免疫偏移有关.
Objective To investigate the effect of echinococcus granulosus antigen B on the severity of streptozotocin induced diabetes mellitus.Methods Thirty male BALB/c mice were randomly divided into 3 groups:echinococcus granulosus antigen B group (group A,n =10),normal saline group (group B,n =10),control group (group C,n =10).Mouse in group A was injected by echinococcus granulosus antigen B and mouse in group B was given normal saline,Type 1 diabetes was induced.After 3 weeks,mice were executed and pancreases were scored on insulitis by HE staining.Serum IFN-γ and IL-4 levels were measured by ELISA.Results After 3 weeks of the establishment of diabetes model mouse body weight in group B and C decreased significantly compared with that in group A.Mouse mean blood glucose level in group A was significantly lower than that in group B and C.There were less than 40% of islets with lymphocytic infiltration in group A,compared with 80% in group B.The average Ridit was 0.423,0.519,and 0.561 in group A,B and C respectively,P < 0.05.IL-4 level in group A was significantly higher than that in group B and group C [(71.6 ± 12.4) ng/ml,(12.6 ± 5.6) ng/ml,(14.2 ± 7.2) ng/ml,P < 0.05].IFN-γ level in group B and group C were higher than that in group A [(276.1 ± 41.7) ng/ml,(352.2 ± 52.2) ng/ml,(358.1 ± 53.4) ng/ml,P < 0.05].Conclusions Type 1 diabetes is organ specific T lymphocyte mediated autoimmune disease.Echinococcus granulosus antigen B has protective effects on diabetes mellitus in mice couteracting autoimmune injury to the islets by streptozotocin,probably by a mechanism related to immune deviation of Th1 to Th2.
出处
《中华普通外科杂志》
CSCD
北大核心
2014年第6期460-463,共4页
Chinese Journal of General Surgery
基金
新疆维吾尔自治区自然科学基金资助项目(2010211B21)