一氧化氮释放阿司匹林衍生物NCX4016在大鼠主动脉中激活可溶性鸟苷酸环化酶的超细胞化学证明。

M G Rambotti, G Mariucci, M Tantucci, M V Ambrosini
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引用次数: 0

摘要

生化研究表明,释放NO的阿司匹林衍生物(NCX4016)通过释放NO刺激人血小板和单核细胞中可溶性鸟苷酸环化酶(sGC)活性,增加环GMP (cGMP)。本研究以硝普钠(0.01 mM)为参比no供体,采用电镜超细胞化学技术研究NCX4016 (2 mM)对大鼠胸主动脉sGC活性的影响。以合成的GTP的不可水解类似物——冠酰亚胺二磷酸钠[Gpp(NH)p]为sGC底物。no活化的sGC释放出与铅离子沉淀的亚胺二磷酸离子,形成电子致密颗粒沉积(反应产物)。超细胞化学证实NCX4016能像硝普钠一样刺激平滑肌细胞,尤其是血管内皮细胞的sGC活性。这一结果可以解释扫描电镜和透射电镜观察到的慢性治疗NCX4016对糖尿病大鼠主动脉内皮的保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ultracytochemical demonstration of soluble guanylate cyclase activation in rat aorta by NCX4016, a NO-releasing aspirin derivative.

Biochemical studies demonstrate that the NO-releasing-aspirin derivative (NCX4016) stimulates soluble guanylate cyclase (sGC) activity and increases cyclic GMP (cGMP) in human platelet and monocytes by releasing NO. In the present study, an ultracytochemical technique for electron microscopy was used to investigate the effects of NCX4016 (2 mM) on sGC activity in rat thoracic aorta, using sodium nitroprusside (0.01 mM) as reference NO-donor. Guanylyl-imidodiphosphate sodium salt [Gpp(NH)p], a synthetic non-hydrolyzable analogue of GTP, was used as sGC substrate. NO-activated sGC released imidodiphosphate ions which were precipitated with lead ions, giving rise to deposits of electron-dense granules (reaction product). Ultracytochemistry allowed us to demonstrate that NCX4016 stimulated sGC activity in smooth muscle cells, and particularly in vascular endothelial cells, as sodium nitroprusside did. This result could explain the protective effects of chronic treatment with NCX4016 on aortic endothelium of diabetic rats demonstrated by scanning and transmission electron microscopy.

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