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目的:探讨细粒棘球蚴抗原B对小鼠1型糖尿病的拮抗作用及其机制。方法:30只雄BALB/c小鼠随机分为三组:肌内注射细粒棘球蚴抗原B加糖尿病成模组(A组,10只);肌内注射生理盐水加糖尿病成模组(B组,10只);对照组(C组,10只)。A组给予细粒棘球蚴抗原B,B组给予相同剂量的生理盐水,均为连续5 d,随后A组、B组均给予小剂量链脲佐菌素诱导1型糖尿病,C组未予任何处理。动态观察血糖变化,至3周末剖杀小鼠,留取血清,取胰腺组织切片HE染色,进行胰岛炎评分,用ELISA测定血清白介素-2(IL-4)、干扰素-γ(IFN-γ)水平。结果:给药后,小鼠血糖逐渐升高,分别在第3天、成模后1周、成模后2周及成模后3周,B组血糖水平分别显著高于A组和C组(P<0.05);A组胰岛可见淋巴细胞浸润不多,而B组胰岛可见较多淋巴细胞浸润;糖尿病模型建立3周末,A组小鼠血清IL-4水平高于B组和C组,差异有统计学意义(P<0.05),A组小鼠血清IFN-γ水平低于B组(P<0.05)。结论:细粒棘球蚴抗原B对小鼠实验性1型糖尿病具有拮抗和保护作用,其机制可能与Th1/Th2免疫偏移有关。
Objective: To investigate the antagonism and mechanism of Echinococcus granulosus antigen B on type 1 diabetes in mice. Methods: Thirty male BALB / c mice were randomly divided into three groups: intramuscular injection of Echinococcus granulosus antigen B plus diabetes mellitus (group A, n = 10); intramuscular injection of saline plus diabetes mellitus (B Group, 10 rats); control group (C group, 10 rats). A group of Echinococcus granulosus antigen B, B group were given the same dose of saline for 5 consecutive days, then A, B group were given low-dose streptozotocin induced type 1 diabetes, C group did not Any deal. The changes of blood glucose were observed dynamically, and the mice were sacrificed at the end of the third week. The serum was collected and the sections of the pancreas were stained with HE for insulitis. Serum levels of interleukin-2 (IL-4) and interferon-γ )Level. Results: After administration, the blood glucose in mice increased gradually. The levels of blood glucose in group B were significantly higher than those in groups A and C at day 3, 1 week after model formation, 2 weeks after model formation, and 3 weeks after model formation, respectively <0.05). A group of islets showed infiltration of lymphocytes, while more islet lymphocytes infiltration was observed in group B; the level of serum IL-4 in group A was higher than that in group B and C Statistically significant (P <0.05). The serum IFN-γ level in group A was lower than that in group B (P <0.05). CONCLUSION: Echinococcus granulosus antigen B can antagonize and protect mice with experimental type 1 diabetes. The mechanism may be related to the Th1 / Th2 immunostaining.