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Nitric oxide modifies glycolytic pathways in cultured human synoviocytes.

机译:一氧化氮修饰了人类滑膜细胞的糖酵解途径。

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Nitric oxide (NO) is a free radical produced during inflammation following activation of an inducible NO synthase by pro-inflammatory cytokines such as IL-1beta. Since both NO and IL-1beta are involved in the physiopathology of inflammatory arthropathies, we investigated the effects of exogenous NO on glycolytic pathways in cultured human osteoarthritic synovial cells. NO generated from S-nitroso-N-acetyl penicillamine (SNAP) or sodium nitroprusside (SNP) inhibited glucose uptake (by 50% after 1 h of incubation) and lactate production by 16% (SNAP) and 8.5% (SNP) after 3 h. Both NO donors also reduced production of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), an enzyme of the glycolytic pathway. This effect was reversed by haemoglobin, a NO scavenger with higher affinity for the radical. In contrast, the effect on glucose uptake appeared to be irreversible. Copyright 2000 Academic Press.
机译:一氧化氮(NO)是在炎症过程中由促炎性细胞因子(例如IL-1beta)激活可诱导的NO合酶后产生的自由基。由于NO和IL-1β均参与炎症性关节病的生理病理,因此我们研究了外源NO对培养的人骨关节炎滑膜细胞糖酵解途径的影响。 S-亚硝基-N-乙酰青霉素胺(SNAP)或硝普钠(SNP)生成的NO抑制葡萄糖摄取(孵育1小时后降低50%),并在3后抑制16%(SNAP)和8.5%(SNP)的乳酸产生H。两位NO供体也减少了糖酵解途径的酶3-磷酸甘油醛脱氢酶(GAPDH)的产生。血红蛋白可以逆转这种作用,血红蛋白是一种对自由基具有更高亲和力的NO清除剂。相反,对葡萄糖摄取的作用似乎是不可逆的。版权所有2000学术出版社。

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