中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2014年
6期
460-463
,共4页
阿依甫汗·阿汗%哈丽娅%吐尔干艾力·阿吉%邵英梅%赵晋明%温浩%曹峻
阿依甫汗·阿汗%哈麗婭%吐爾榦艾力·阿吉%邵英梅%趙晉明%溫浩%曹峻
아의보한·아한%합려아%토이간애력·아길%소영매%조진명%온호%조준
糖尿病,实验性%细粒棘球绦虫%Th1细胞%Th2细胞
糖尿病,實驗性%細粒棘毬縚蟲%Th1細胞%Th2細胞
당뇨병,실험성%세립극구조충%Th1세포%Th2세포
Mellitus diabetes,experimental%Echinococcus granulosus%Th1 cells%Th2 cells
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.
目的 探討細粒棘毬蚴抗原B對小鼠1型糖尿病髮病的早期影響及其機製.方法 30隻BALB/c小鼠隨機分組:細粒棘毬蚴抗原B+糖尿病組(A組);生理鹽水+糖尿病組(B組);糖尿病組(C組);A組給予細粒棘毬蚴抗原B,B組給予生理鹽水,隨後A、B、C組均給予小劑量鏈脲佐菌素誘導1型糖尿病.觀察血糖變化,留取標本進行細胞因子等指標測定.結果 在糖尿病成模後3週,A組<40%的胰島可見淋巴細胞浸潤,B組和C組有80%的胰島見淋巴細胞浸潤,差異有統計學意義(A組、B組和C組的平均Ridit值分彆為:0.423、0.519、0.561,P<0.05);糖尿病模型建立3週末,A組小鼠血清白細胞介素-4(IL-4)水平高于B組和C組[(71.6±12.4) ng/ml比(12.6±5.6) ng/ml和(14.2-7.2) ng/ml,P<0.05],A組小鼠血清γ-榦擾素(IFN-γ)水平低于B組和C組[(276.1 ±41.7) ng/ml比(352.2±52.2)ng/ml和(358.1 ±53.4) ng/ml,P<0.05]. 結論 細粒棘毬蚴抗原B對小鼠1型糖尿病早期胰島細胞的自身免疫損害具有拮抗作用,其機製可能與Th1/Th2免疫偏移有關.
목적 탐토세립극구유항원B대소서1형당뇨병발병적조기영향급기궤제.방법 30지BALB/c소서수궤분조:세립극구유항원B+당뇨병조(A조);생리염수+당뇨병조(B조);당뇨병조(C조);A조급여세립극구유항원B,B조급여생리염수,수후A、B、C조균급여소제량련뇨좌균소유도1형당뇨병.관찰혈당변화,류취표본진행세포인자등지표측정.결과 재당뇨병성모후3주,A조<40%적이도가견림파세포침윤,B조화C조유80%적이도견림파세포침윤,차이유통계학의의(A조、B조화C조적평균Ridit치분별위:0.423、0.519、0.561,P<0.05);당뇨병모형건립3주말,A조소서혈청백세포개소-4(IL-4)수평고우B조화C조[(71.6±12.4) ng/ml비(12.6±5.6) ng/ml화(14.2-7.2) ng/ml,P<0.05],A조소서혈청γ-간우소(IFN-γ)수평저우B조화C조[(276.1 ±41.7) ng/ml비(352.2±52.2)ng/ml화(358.1 ±53.4) ng/ml,P<0.05]. 결론 세립극구유항원B대소서1형당뇨병조기이도세포적자신면역손해구유길항작용,기궤제가능여Th1/Th2면역편이유관.
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.