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首页> 外文期刊>American Journal of Physiology >Pentoxifylline protects against endotoxin-induced acute renal failure in mice.
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Pentoxifylline protects against endotoxin-induced acute renal failure in mice.

机译：己酮可可碱可防止内毒素引起的小鼠急性肾功能衰竭。

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Acute renal failure (ARF) in septic patients drastically increases the mortality to 50-80%. Sepsis induces several proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), a major pathogenetic factor in septic ARF. Pentoxifylline has several functions including downregulation of TNF-alpha and endothelia-dependent vascular relaxation. We hypothesized that pentoxifylline may afford renal protection during endotoxemia either by downregulating TNF-alpha and/or by improving endothelial function. In wild-type mice, pentoxifylline protected against the fall in glomerular filtration rate (GFR; 105.2 +/- 6.6 vs. 50.2 +/- 6.6 microl/min, P < 0.01) at 16 h of LPS administration (2.5 mg/kg ip). This renal protective effect of pentoxifylline was associated with an inhibition of the rise in serum TNF-alpha (1.00 +/- 0.55 vs. 7.02 +/- 2.40 pg/ml, P < 0.05) and serum IL-1beta (31.3 +/- 3.6 vs. 53.3 +/- 5.9 pg/ml, P < 0.01) induced by LPS. Pentoxifylline also reversed the LPS-related increase in renal iNOS and ICAM-1 and rise in serum nitric oxide (NO). Enhanced red blood cell deformability by pentoxifylline may have increased shear rate and upregulated eNOS. Studies were therefore performed in eNOS knockout mice. The renal protection against endotoxemia with pentoxifylline was again observed as assessed by GFR (119.8 +/- 18.0 vs. 44.5 +/- 16.2 microl/min, P < 0.05) and renal blood flow (0.86 +/- 0.08 vs. 0.59 +/- 0.05 ml/min, P < 0.05). Renal vascular resistance significantly decreased with the pentoxifylline (91.0 +/- 5.8 vs. 178.0 +/- 7.6 mmHg.ml(-1).min(-1), P < 0.01). Thus pentoxifylline, an FDA-approved drug, protects against endotoxemia-related ARF and involves a decrease in serum TNF-alpha, IL-1beta, and NO as well as a decrease in renal iNOS and ICAM-1.
机译：败血病患者的急性肾衰竭（ARF）极大地提高了死亡率至50-80％。脓毒症诱导几种促炎细胞因子，包括肿瘤坏死因子-α（TNF-alpha），这是脓毒症ARF中的主要致病因素。己酮可可碱具有几种功能，包括下调TNF-α和内皮依赖性血管舒张。我们假设己酮可可碱在内毒素血症期间可通过下调TNF-α和/或改善内皮功能来提供肾脏保护。在野生型小鼠中，己酮可可碱在LPS给药（2.5 mg / kg ip）时可防止肾小球滤过率下降（GFR; 105.2 +/- 6.6与50.2 +/- 6.6 microl / min，P <0.01） ）。己酮可可碱的这种肾脏保护作用与抑制血清TNF-α（1.00 +/- 0.55 vs. 7.02 +/- 2.40 pg / ml，P <0.05）和血清IL-1beta（31.3 +/-）升高有关由LPS诱导的3.6 vs.53.3 +/- 5.9 pg / ml，P <0.01）。己酮可可碱还逆转了LPS相关的肾脏iNOS和ICAM-1的增加以及血清一氧化氮（NO）的增加。己酮可可碱增强红细胞的可变形性可能会增加剪切速率并上调eNOS。因此，在eNOS基因敲除小鼠中进行了研究。通过GFR（119.8 +/- 18.0 vs. 44.5 +/- 16.2 microl / min，P <0.05）和肾血流量（0.86 +/- 0.08 vs. 0.59 + /）再次评估了己酮可可碱对内毒素血症的肾脏保护作用-0.05毫升/分钟，P <0.05）。己酮可可碱的肾血管阻力显着降低（91.0 +/- 5.8与178.0 +/- 7.6 mmHg.ml（-1）.min（-1），P <0.01）。因此，己酮可可碱（一种已获FDA批准的药物）可预防内毒素血症相关的ARF，并涉及血清TNF-α，IL-1β和NO的降低以及肾脏iNOS和ICAM-1的降低。

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