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首页> 外文期刊>Life sciences >Inhibitory effect of naringin on lipopolysaccharide (LPS)-induced endotoxin shock in mice and nitric oxide production in RAW 264.7 macrophages
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Inhibitory effect of naringin on lipopolysaccharide (LPS)-induced endotoxin shock in mice and nitric oxide production in RAW 264.7 macrophages

机译：柚皮苷对脂多糖（LPS）诱导的小鼠内毒素休克的抑制作用以及RAW 264.7巨噬细胞中一氧化氮的产生

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摘要

Lipopolysaccharide (LPS) has been known to induce endotoxin shock via production of inflammatory modulators such as tumor necrosis factor alpha (TNF-alpha), or nitric oxide (NO). In this study, we have examined the effect of naringin (NG), one of the flavonoids, on LPS-induced endotoxin shock in mice and NO production in RAW 264.7 macrophages. For intraperitoneal (i.p., 20 mg/kg) injection of LPS at 48 h, the survival rate of mice administered with LPS alone (n = 10) or pretreated with NG at 10, 30 and 60 mg/kg (i.p.) group (n = 10) was 0% or 10%, 50% and 70%, respectively. NG dose-dependently suppressed LPS-induced production of TNF-a. LPS-induced production of NO at 6 h (125.89 +/- 16.35 mu M), as measured by nitrite formation, was significantly reduced by NG at 30 or 60 mg/kg for 49.49 +/- 4.81 or 27.91 +/- 1.81 mu M (P < 0.01 vs. LPS alone), respectively. To further examine the mechanism by which NG suppresses LPS-induced endotoxin shock, we used an in vitro model, RAW 264.7 mouse macrophage cells. NG (I mM) suppressed LPS (0.01, 0.1 or 1 mu g/ml)-induced production of NO and the expression of inflammatory gene products such as inducible NO synthase (iNOS), TNF-a, inducible cyclooxygenase (COX-2) and interleukin-6 (IL-6) as determined by RT-PCR assay. NG was found to have blocked the LPS-induced transcriptional activity of NF-KB in electrophoretic mobility shift assay and reporter assay. These findings suggest that suppression of the LPS-induced mortality and production of NO by NG is due to inhibition of the activation of NF-KB. (c) 2005 Elsevier Inc. All rights reserved.
机译：已知脂多糖（LPS）通过产生炎性调节剂如肿瘤坏死因子α（TNF-α）或一氧化氮（NO）来诱导内毒素休克。在这项研究中，我们已经检查了柚皮素（NG）（一种类黄酮）对LPS诱导的小鼠内毒素休克和RAW 264.7巨噬细胞中NO产生的影响。对于在48 h腹腔内（ip，20 mg / kg）注射LPS，单独给予LPS（n = 10）或经NG预处理的小鼠在10、30和60 mg / kg（ip）组的存活率（n = 10）分别为0％或10％，50％和70％。 NG剂量依赖性地抑制LPS诱导的TNF-α的产生。通过亚硝酸盐形成测量，LPS诱导的6 h（125.89 +/- 16.35μM）下NO生成的NO在30或60 mg / kg的NG下显着降低了49.49 +/- 4.81或27.91 +/- 1.81 mu的NO生成M（分别为P <0.01与LPS）。为了进一步研究NG抑制LPS诱导的内毒素休克的机制，我们使用了体外模型RAW 264.7小鼠巨噬细胞。 NG（1 mM）抑制LPS（0.01、0.1或1μg / ml）诱导的NO产生以及炎症基因产物的表达，例如诱导型NO合酶（iNOS），TNF-α，诱导型环氧合酶（COX-2）通过RT-PCR分析确定白介素6（IL-6）。在电泳迁移率迁移分析和报告基因分析中，发现NG阻断了LPS诱导的NF-KB转录活性。这些发现表明NG抑制LPS诱导的死亡率和NO的产生是由于抑制了NF-KB的活化。 （c）2005 Elsevier Inc.保留所有权利。

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