Effect of echinococcus granulosus antigen B on streptozotocin induced diabetes mellitus in mice
10.3760/cma.j.issn.1007-631X.2014.06.015
- VernacularTitle:细粒棘球蚴抗原B对小鼠早期实验性1型糖尿病的影响
- Author:
Ayifuhan AHAN
;
Tuerganaili AJI
;
Yingmei SHAO
;
Jinming ZHAO
;
Hao WEN
;
Jun CAO
- Publication Type:Journal Article
- Keywords:
Mellitus diabetes,experimental;
Echinococcus granulosus;
Th1 cells;
Th2 cells
- From:
Chinese Journal of General Surgery
2014;29(6):460-463
- CountryChina
- Language:Chinese
-
Abstract:
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.