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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Induction of heat shock protein 72 by a nitric oxide donor in guinea-pig gastric mucosal cells.
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Induction of heat shock protein 72 by a nitric oxide donor in guinea-pig gastric mucosal cells.

机译:一氧化氮供体在豚鼠胃粘膜细胞中诱导热休克蛋白72。

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摘要

Gastric mucosal cells may be exposed to exogenous nitric oxide (NO) from a variety of sources. The response of primary cultures of guinea-pig gastric mucosal cells to the NO donor S-nitroso-N-acetyl-penicillamine was therefore investigated. Exposure to S-nitroso-N-acetyl-penicillamine for 8 h caused a concentration-dependent induction of heat shock protein 72 (HSP 72). Induction was inhibited by the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, and by blockade of transcription with actinomycin D. Induction of HSP 72 by S-nitroso-N-acetyl-penicillamine was enhanced by diethyl maleate which decreased the intracellular reduced thiol content. By contrast, HSP 72 formation after heat shock was associated with an elevation of reduced thiol. Incubation with S-nitroso-N-acetyl-penicillamine for 18 h increased detachment of cells from the culture plate. The effect of S-nitroso-N-acetyl-penicillamine on detachment was exacerbated by the presence of actinomycin D. In conclusion, exogenous NO induces HSP 72 in guinea-pig gastric mucosal cells and this response may in part protect the cells from the deleterious effects of NO.
机译:胃粘膜细胞可能会接触各种来源的外源性一氧化氮(NO)。因此,研究了豚鼠胃粘膜细胞原代培养物对NO供体S-亚硝基-N-乙酰基-青霉胺的反应。暴露于S-亚硝基-N-乙酰青霉胺8 h引起热休克蛋白72(HSP 72)的浓度依赖性诱导。 NO清除剂2-(4-羧基苯基)-4,4,5,5-四甲基咪唑啉-1-氧基1-3氧化物以及放线菌素D的转录阻滞抑制了诱导。S-亚硝基诱导HSP 72马来酸二乙酯增强了-N-乙酰基青霉胺的含量,从而降低了细胞内硫醇的含量。相比之下,热冲击后HSP 72的形成与硫醇还原的升高有关。与S-亚硝基-N-乙酰基-青霉胺一起孵育18小时可增加细胞与培养板的分离。放线菌素D的存在会加剧S-亚硝基-N-乙酰基-青霉胺对脱落的影响。总之,外源NO诱导豚鼠胃粘膜细胞中的HSP 72,这种反应可能部分保护细胞免受有害NO的影响

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