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首页> 外文期刊>Functional Foods In Health And Disease >Effects of medicinal plant ipe on expression of inducible nitric oxide synthase in inerleukin-1β-stimulated Hepatocytes
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Effects of medicinal plant ipe on expression of inducible nitric oxide synthase in inerleukin-1β-stimulated Hepatocytes

机译：药用植物ipe对IL-1β刺激的肝细胞诱导型一氧化氮合酶表达的影响

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Background: The traditional medicine ipe is thought to have various pharmacological actions including anticancer and anti-inflammatory activities. However, there is little scientific evidence to demonstrate the organ-protective effects of ipe. The prevention of nitric oxide (NO) production in inflamed livers by inducible NO synthase (iNOS) is an indicator of liver protection. We examined proinflammatory cytokine-stimulated hepatocytes as a simple “in vitro liver injury model” to determine ipe’s liver-protective effects of ipe and clarify its mechanisms. This study aims to examine whether ipe influences iNOS induction and NO production, and if so, the mechanisms involved in its action.Methods: Primary cultured hepatocytes were treated with interleukin (IL)-1β in the presence or absence of ipe. The induction of iNOS and its signal pathway were analyzed.Results: Ipe inhibited the production of NO stimulated by IL-1β and showed the greatest effect (more than 90% inhibition) at 2 mg/ml. Ipe decreased iNOS protein and mRNA expression. Ipe decreased NF-κB activation (its translocation to the nucleus and DNA binding), although there was no effect on IκBα degradation. Ipe inhibited Akt activation, followed by decreased the type I IL-1 receptor mRNA and protein levels. Transfection experiments revealed that ipe decreased both activities of iNOS promoter transactivation and mRNA stability. In support of the latte observation, ipe inhibited the expression of the antisense transcript of the iNOS gene.Conclusion: Ipe blocked IκB kinase and phosphatidylinositol 3-kinase/Akt signal pathways, which caused the reduction of iNOS mRNA synthesis and its stability. This resulted in the inhibition of iNOS induction and NO production. Ipe may have a potent beneficial effect against NO-mediated injury in organs including the liver.
机译：背景：传统的中药被认为具有多种药理作用，包括抗癌和消炎作用。但是，几乎没有科学证据证明ipe的器官保护作用。诱导型一氧化氮合酶（iNOS）预防发炎的肝脏中一氧化氮（NO）的产生是肝脏保护的指标。我们检查了促炎细胞因子刺激的肝细胞，将其作为简单的“体外肝损伤模型”，以确定ipe对ipe的肝保护作用并阐明其机理。这项研究的目的是检查ipe是否会影响iNOS的诱导和NO的产生，以及是否影响iNOS的作用。方法：在有或没有ipe的情况下，用白介素（IL）-1β处理原代培养的肝细胞。结果：Ipe抑制了IL-1β刺激的NO生成，在2 mg / ml时表现出最大的抑制作用（抑制率超过90％）。 Ipe降低了iNOS蛋白和mRNA表达。 Ipe降低了NF-κB活化（其易位至细胞核和DNA结合），尽管对IκBα降解没有影响。 Ipe抑制Akt激活，然后降低I型IL-1受体mRNA和蛋白水平。转染实验表明，ipe降低了iNOS启动子反式激活的活性和mRNA的稳定性。结论：Ipe阻断了IκB激酶和磷脂酰肌醇3-激酶/ Akt信号通路，从而导致iNOS mRNA合成及其稳定性的降低，从而支持itteS基因反义转录的表达。这导致iNOS诱导和NO产生的抑制。 Ipe可能对包括肝脏在内的器官中的NO介导的损伤具有有效的有益作用。

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