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首页> 外文期刊>Biochemistry >Production of Heat Shock Proteins,Cytokines,and Nitric Oxide in Toxic Stress
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Production of Heat Shock Proteins,Cytokines,and Nitric Oxide in Toxic Stress

机译:在有毒胁迫下产生热激蛋白,细胞因子和一氧化氮

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摘要

Expression of heat shock proteins Hsp27,Hsp90,and Hsp70 and production of tumor necrosis factors(TNF-alpha,TNF-beta),interferon-gamma(IFN-gamma),interleukin-2,-3,-6,and nitric oxide(NO)were studied under conditions of acute and chronic intoxication of animals with lipopolysaccharides.Injection of endotoxin increased expression of heat shock proteins Hsp70 and Hsp90-alpha in mouse cells.Acute toxic stress also provoked a sharp increase in the production of TNF-alpha,TNF-beta,and NO in mouse cells.The production of other cytokines(interleukins and IFN-gamma)was changed insignificantly.In the model of chronic toxic stress,changes in the production of Hsp70,Hsp90,TNF,and NO were followed during 11 days after the beginning of the toxin injections.The expression of Hsp70 and Hsp90 in acute stress was significantly higher than at the final stage of the chronic exposure.The changes in the TNF and NO productions,on one hand,and the production of heat shock proteins,on the other hand,were synchronous.The findings indicate that repeated injections of increasing endotoxin doses result in a decreased ability of the body cells to respond to stress by overproduction of heat shock proteins,TNF,and NO.
机译:热休克蛋白Hsp27,Hsp90和Hsp70的表达以及肿瘤坏死因子(TNF-alpha,TNF-beta),干扰素-γ(IFN-γ),白介素-2,-3,-6和一氧化氮的产生在脂多糖对动物的急性和慢性中毒条件下进行了研究。注射内毒素会增加小鼠细胞中热休克蛋白Hsp70和Hsp90-α的表达;急性毒性应激也导致TNF-α的产生急剧增加,小鼠细胞中的TNF-beta和NO。其他细胞因子(白介素和IFN-γ)的产生变化不明显。在慢性毒性应激模型中,Hsp70,Hsp90,TNF和NO的产生在随后的过程中发生了变化。毒素注射开始后的第11天,急性应激中Hsp70和Hsp90的表达明显高于慢性暴露的最后阶段。一方面,TNF和NO产生以及热量产生的变化另一方面,休克蛋白是同步的研究结果表明,反复注射增加剂量的内毒素会导致人体细胞通过过度产生热休克蛋白,TNF和NO而降低对应激的反应能力。

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