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机构地区:[1]山东省济宁医学院附属医院内分泌科,河南医科大学,省医学科学研究所肝炎组
出 处:《中国糖尿病杂志》1996年第4期212-214,共3页Chinese Journal of Diabetes
摘 要:将新发病的IDDM病人周围血单个核细胞(PBMC)同大鼠胰岛共同培养20个小时后用L-精氨酸刺激,收集并测定基础和刺激后培养上清中胰岛素的含量,结果显示:IDDM病人PBMC作用下的基础胰岛素释放(117.9±14.0±μU·10islets-1/20h)(n=11)和刺激后胰岛素释放(147.5±32.3μU·10islets-1/3h)(n=11),显著低于正常人PBMC作用下的基础胰岛素释放(184.8±29.5μU)(n=10,P<0.01)和刺激后胰岛素释放(195.0±27.4μU)(n=10,P<0.01)。结果表明新发病的IDDM病人PBMC能够抑制大鼠胰岛基础和刺激后胰岛素的释放。The pancreatic islets isolated from rats by collegenase, and purified by Ficoll-Densitygradient-centrifugation,were incubated for about 20 hrs in DMEM with peripheral blood mononuclear cells(PBMCs)of newly onset IDDM.Then,the islets were stimulated by L-arginine(10mmol/L)in DMEM.The supernatant were taken before and after stimulation for detecting insulin by radioimmunoassay as basic and stimulated insulin release.The results were as follows:In the presence of PBMCs from IDDM patients:the mean basic insulin release was 117.9±14.0μU·10 islets-1/20h(n=11).It was significantly lower than corresponding results(184. 8±29.5μU·10 islets-1/20h)(n=10,P<0.01)in the presence of control PBMCs.The mean stimulated insulin release of 147.5±32.3μU·10 1slets-1/3h from IDDM group was significantly lower than the corresponding release of 195.0±27.4μU ·10 islets-1/3h of the control group(P<0.01).Our results display that the PBMCs of IDDM may inhibit the basic and stimulated insulin release of islets, and demonstrate that the cell-mediated immunity disturbance may play a role in the pathogenesis of IDDM.
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