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硝苯地平通过下调 NFkB 抑制低氧诱导的跨血管渗漏。

Nifedipine inhibits hypoxia induced transvascular leakage through down regulation of NFkB.

机构信息

Department of Experimental Biology, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi 54, India.

出版信息

Respir Physiol Neurobiol. 2012 Jul 31;183(1):26-34. doi: 10.1016/j.resp.2012.05.016. Epub 2012 May 22.

Abstract

We have studied the prophylactic administration of nifedipine and its molecular mechanism involved in reducing the transvascular leakage and inflammation in rats under hypoxia. Rats exposed to an altitude of 7620m for 6h resulted into significant increase in transvascular leakage, oxidative stress with increased NFkB expression in lungs followed by significant increase in pro inflammatory cytokines (IL-1, TNF-α) with up regulation of cell adhesion molecules (ICAM-I, VCAM-I, E-selectin, and P-selectin) in the lungs over control. Prophylactic administration of nifedipine significantly reduced the transvascular leakage, oxidative stress, inhibited the up regulation of NFkB in lungs of rats compared to control. In addition, nifedipine significantly suppressed the levels of proinflammatory cytokines and cell adhesion molecules and stabilized the HIF1-α accumulation in the lungs of rats compared to control. These results indicate that, nifedipine has an inhibitory effect on initial leaking and showed reduction in progression of inflammation through down regulation of NFkB activity in lungs of rats under hypoxia.

摘要

我们研究了硝苯地平的预防给药及其在降低缺氧大鼠血管外渗漏和炎症中的分子机制。将大鼠暴露于 7620 米的高海拔 6 小时后,会导致肺血管外渗漏显著增加,氧化应激导致 NFkB 表达增加,随后炎症细胞因子(IL-1、TNF-α)显著增加,细胞黏附分子(ICAM-1、VCAM-1、E-选择素和 P-选择素)在肺中的表达上调。与对照组相比,硝苯地平的预防给药可显著减少大鼠的血管外渗漏和氧化应激,抑制 NFkB 在肺中的上调。此外,与对照组相比,硝苯地平还可显著抑制炎症细胞因子和细胞黏附分子的水平,并稳定缺氧大鼠肺中的 HIF1-α积累。这些结果表明,硝苯地平对初始渗漏具有抑制作用,并通过下调 NFkB 在缺氧大鼠肺中的活性来减少炎症的进展。

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