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Nitric Oxide-dependent Pathway Regulates Granulocytes Cytokines Release in Cultured Human Leucocytes from -II Diabetes Mellitus

机译:一氧化氮依赖性途径调节粒细胞细胞因子在-II糖尿病中培养的人白细胞释放

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The mechanism of release of proinflammatory cytokines by blood granulocytes in diabetes is unknown., We investigated whether diabetes mellitus affects the production of cytokines by granulocytes (PMN) and mononuclear cells (PBMC) and whether this is modulated by NO Isolated PMN and PBMC from with or without type-II diabetes mellitus were incubated at 37degC for 6h with S-nitroso-N-acetylpenicillamine (SNAP) at 0, 1, and IOOlxM with or without lipopolysaccharides (LPS) stimulation (1mug/mL). Supernatants were assayed for tumor necrosis factor-a (TNF-a) and interleukin-8 (IL-8) by sandwich ELISA, Significant increases in TNF-a and IL-8 were observed only in PMN from diabetic subjects with or without LPS stimulation and that exogenous NO inhibited further production of cytokines in a concentration dependent manner, However, activity of PBMC when stimulated with LPS was greatly enhanced by diabetes, but not affected by NO production. Hence, suggesting that granulocytes activation and participation in diabetes related complications is modulated by NO bioavailability.
机译:糖尿病中血粒细胞释放促炎细胞因子的机制是未知的。,我们研究了糖尿病的糖尿病吗啡(PMN)和单核细胞(PBMC)产生细胞因子的产生,以及是否通过没有分离的PMN和PBMC来调节或者没有类型-II型糖尿病,在37degc下用S-Nitroso-N-乙酰戊酰胺(Snap)温育6h,在0,1和与脂多糖(LPS)刺激(1Mug / ml)的IOOLXM。通过夹心ELISA测定肿瘤坏死因子-A(TNF-A)和白细胞介素-8(IL-8)的上清液,仅在糖尿病受试者的PMN中观察到TNF-A和IL-8的显着增加,或没有LPS刺激并且外源不会抑制浓度依赖性方式的细胞因子的进一步产生细胞因子,然而,当用LPS刺激时,PBMC的活性大大提高了糖尿病,但不受没有生产的影响。因此,表明粒细胞激活和参与糖尿病相关并发症的不含生物利用度。

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