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Inducible nitric oxide synthase mediates cytokine release: the time course in conscious and septic rats.

机译:诱导型一氧化氮合酶介导细胞因子释放:在有意识和脓毒症的大鼠中的时间过程。

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Nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), and interleukin 1-beta (IL-1beta) are postulated to play a key pathophysiologic role during sepsis. In this study, we examined the time course of inducible NO synthase (iNOS) mRNA expression and the plasma TNF-alpha and IL-1beta in lipopolysaccharide (LPS)-treated conscious rats. The hemodynamic pattern in septic shock is more similar to clinical conditions without anesthesia. The data showed that a significant increase in iNOS mRNA levels was found in the spleen, lung, liver, with slight elevation in the heart and kidney at 3 h after LPS administration. However, iNOS mRNA levels were not elevated significantly in all tissues examined at 24 h. In the plasma, TNF-alpha and IL-1beta culminated within 1 h, and reduced gradually to baseline levels in a relatively short period (within 9 h). The results suggest that local NO production by activation of iNOS mRNA expression and cytokine release may contribute to LPS-induced organ dysfunction at various time points.
机译:一氧化氮(NO),肿瘤坏死因子-α(TNF-alpha)和白介素1-beta(IL-1beta)被假定在败血症中起关键的病理生理作用。在这项研究中,我们检查了诱导性NO合酶(iNOS)mRNA表达的时间过程以及脂多糖(LPS)治疗的清醒大鼠的血浆TNF-alpha和IL-1beta。败血性休克的血流动力学模式与没有麻醉的临床情况更为相似。数据显示,LPS给药3小时后,脾脏,肺脏,肝脏中iNOS mRNA水平显着增加,心脏和肾脏略有升高。然而,在24小时检查的所有组织中,iNOS mRNA水平并未显着升高。在血浆中,TNF-α和IL-1β在1小时内达到顶点,并在较短的时间内(9小时内)逐渐降低至基线水平。结果表明,通过激活iNOS mRNA表达和细胞因子释放引起的局部NO产生可能在不同时间点导致LPS诱导的器官功能障碍。

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