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钙果硼酸酯对 LPS 刺激的 RAW264.7 巨噬细胞产生炎症介质的体外影响。

In vitro effects of calcium fructoborate upon production of inflammatory mediators by LPS-stimulated RAW 264.7 macrophages.

机构信息

Department of Biochemistry, University of Craiova, 13 AI Cuza, 200585 Craiova, Romania.

出版信息

Biol Trace Elem Res. 2010 Jun;135(1-3):334-44. doi: 10.1007/s12011-009-8488-5. Epub 2009 Aug 11.

Abstract

The present study is supported by our previous findings suggesting that calcium fructoborate (CF) has anti-inflammatory and antioxidant properties. Thus, we investigated the effects of CF on a model for studying inflammatory disorders in vitro represented by lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264.7 cells. This investigation was performed by analyzing the levels of some mediators released during the inflammatory process: cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukins IL-1beta and IL-6 as well as cyclooxygenase-2 (COX-2), the main enzyme responsible for endotoxin/LPS-induced prostaglandin synthesis by macrophages. We also measured production of nitric oxide (NO) that plays an important role in the cytotoxicity activity of macrophages towards microbial pathogens. After CF treatment of LPS-stimulated macrophages we found an up-regulation of TNF-alpha protein level in culture medium, no significant changes in the level of COX-2 protein expression and a decrease in NO production as well as in IL-1beta and IL-6 release. Collectively, this series of experiments indicate that CF affect macrophage production of inflammatory mediators. However, further research is required in order to establish whether CF treatment can be beneficial in suppression of pro-inflammatory cytokine production and against progression of endotoxin-related diseases.

摘要

本研究是基于我们之前的研究结果,表明果聚糖硼酸钙(CF)具有抗炎和抗氧化特性。因此,我们研究了 CF 对脂多糖(LPS)刺激的鼠巨噬细胞 RAW 264.7 细胞体外炎症模型的影响。通过分析炎症过程中释放的一些介质的水平来进行这项研究:细胞因子如肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)以及环氧化酶-2(COX-2),后者是巨噬细胞中内毒素/LPS 诱导前列腺素合成的主要酶。我们还测量了一氧化氮(NO)的产生,NO 在巨噬细胞对微生物病原体的细胞毒性活性中起重要作用。在用 CF 处理 LPS 刺激的巨噬细胞后,我们发现培养基中 TNF-α蛋白水平上调,COX-2 蛋白表达水平无显著变化,NO 产生以及 IL-1β和 IL-6 的释放减少。总的来说,这一系列实验表明 CF 影响巨噬细胞炎症介质的产生。然而,需要进一步的研究来确定 CF 治疗是否能抑制促炎细胞因子的产生,并防止内毒素相关疾病的进展。

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