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作 者:王占科[1] 何凤田[2] 许霖水[2] 汪仕良[3] 雷万生[1] 唐小平[1] 熊晓平[1]
机构地区:[1]解放军第九四医院创伤研究室,江西南昌330002 [2]第三军医大学基础部生物化学与分子生物学教研室,重庆400038 [3]第三军医大学解放军烧伤研究所,创伤、烧伤与复合伤国家重点实验室,重庆400038
出 处:《肠外与肠内营养》2008年第4期193-196,共4页Parenteral & Enteral Nutrition
基 金:江西省卫生厅资助课题(20052044);南京军区医药卫生“十一五”资助重大课题(06Z25);南京军区卫生专业人才培养“122工程”资助项目
摘 要:目的:观察葡萄糖钾盐是否具有协同增强胰岛素对外周血单个核细胞群(PBMCs)分泌促炎细胞因子和抗炎细胞因子的作用。方法:用Ficoll-Hypaque液分离10例健康人PBMC,随机分为胰岛素葡萄糖钾盐(GIK)组、胰岛素(INS)组、葡萄糖钾盐(GK)组和基础对照(C)组。四组PBMC培养24 h后,加脂多糖继续培养48 h后,离心收集培养上清液。用ELISA法检测TNF-α,IL-6和IL-4,IL-10含量。结果:GIK组和INS组TNF-α,IL-6含量均明显低于C组(P<0.01),IL-4和IL-10含量却均明显高于C组(P<0.01);GIK组IL-4和IL-10含量明显高于INS组(P<0.01),但GIK组TNF-α和IL-6含量降低,与INS组比较无统计学意义(P>0.05)。结论:胰岛素葡萄糖钾盐和胰岛素均能直接抑制内毒素刺激的PBMCs分泌促炎细胞因子,同时提高内毒素刺激的PBMC分泌抗炎细胞因子水平。葡萄糖钾盐对胰岛素促进PBMCs分泌抗炎细胞因子有协同增强作用。Objective :To explore whether the glucose-Potassium enhances the effects of insulin on the production of pre-inflammation and anti-inflammation cytokines by peripheral blood mononuclear cells (PBMCs) in vitro. Methods: The PBMCs were isolated by nonconsecutive gradient centrifugating methods with Ficoll-Hypaque solution[Density=(0.077±0.001)g/ml] from 10 healthy donators and divided randomly to insulin-glucose- potassium group(GIK group, n=24), insulin group(INS group, n=24) , glucose-potassium group(GK group, n=24) and control group( C group, n=24). The PBMCs of four groups were incubated for 24 hours at 37℃ and 5% CO2 in RPMI 1640 solution, and after lipopo-lysaccharide added, they were incubated for 48 hours at same condition. The supernatants of PBMCs were collected to detect the pre-inflammation cytokines of TNF-α and IL-6 and anti-inflammation cytokines of IL-4, IL-10 by ELISA. Results: The levels of TNF-α and IL-6 in the supernatants of PBMCs of GIK and INS groups were significantly lower than thase of C group(P 〈0.01), and the IL-4 and IL-10 levels of GIK and INS groups were significantly higher than those of C group(P〈0.01). The IL-4 and IL-10 levels in supernatants of PBMCs of the GIK group were significantly higher than those of INS group (P 〈 0.01 ), but the TNF-α and IL-6 levels of GIK group were not lower than those of INS group (P〉0.05). Conclusion: Insulin-glucose-potassium or insulin may inhibit the pre-inflammation cytokines and enhance anti-inflammation cytokines production of PBMCs stimulated with LPS directly. Glucose-potassium may enhance the effects of insulin on the elevated production of anti-inflammation cytokines of PBMCs stimulated with LPS.
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