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熊果苷对脂多糖刺激的 BV2 小胶质细胞的抗炎作用。

Anti-inflammatory effects of arbutin in lipopolysaccharide-stimulated BV2 microglial cells.

机构信息

College of Pharmacy, Inje University, Gimhae, Gyungnam, South Korea.

出版信息

Inflamm Res. 2012 Aug;61(8):817-25. doi: 10.1007/s00011-012-0474-2. Epub 2012 Apr 10.

Abstract

OBJECTIVES AND DESIGN

Arbutin, which is found in the genus Arctostaphylos, is an anti-oxidant and a depigmenting agent. The present study was designed to validate the anti-inflammatory effect of arbutin.

MATERIALS AND METHODS

The anti-inflammatory properties of arbutin were studied using a lipopolysaccharide (LPS)-stimulated murine BV2 microglial cells model. As inflammatory parameters, the production of nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) were evaluated. We also examined the expression of ninjurin1 (Ninj1) and the adhesion activity of BV2 cells. Finally, we analyzed the activation of the nuclear factor-κB (NF-κB) signaling pathway.

RESULTS

Arbutin suppressed LPS-induced production of NO and expression of iNOS and COX-2 in a dose-dependent manner without causing cellular toxicity. Arbutin also significantly reduced generation of proinflammatory cytokines, including IL-1β and TNF-α, and other inflammation-related genes such as MCP-1 and IL-6. Additionally, arbutin suppressed the adhesion activity of BV2 cells and the expression of an important adhesion molecule, Ninj1, in LPS-stimulated murine BV2 cells. Furthermore, arbutin inhibited nuclear translocation and the transcriptional activity of NF-κB.

CONCLUSIONS

Taken together, our results suggest that arbutin might be useful for treating the inflammatory and deleterious effects of BV2 microglial cells activation in response to LPS stimulation.

摘要

目的和设计

熊果苷存在于熊果酸属中,是一种抗氧化剂和脱色剂。本研究旨在验证熊果苷的抗炎作用。

材料和方法

使用脂多糖 (LPS) 刺激的小鼠 BV2 小胶质细胞模型研究熊果苷的抗炎特性。作为炎症参数,评估了一氧化氮 (NO)、诱导型一氧化氮合酶 (iNOS)、环氧合酶-2 (COX-2)、肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)、单核细胞趋化蛋白-1 (MCP-1) 和白细胞介素-6 (IL-6) 的产生。我们还检查了 ninjurin1 (Ninj1) 的表达和 BV2 细胞的粘附活性。最后,我们分析了核因子-κB (NF-κB) 信号通路的激活。

结果

熊果苷以剂量依赖的方式抑制 LPS 诱导的 NO 产生和 iNOS 和 COX-2 的表达,而不会引起细胞毒性。熊果苷还显著降低了包括 IL-1β 和 TNF-α 在内的促炎细胞因子以及其他炎症相关基因(如 MCP-1 和 IL-6)的产生。此外,熊果苷抑制了 LPS 刺激的小鼠 BV2 细胞中 BV2 细胞的粘附活性和重要粘附分子 Ninjurin1 的表达。此外,熊果苷抑制了 NF-κB 的核转位和转录活性。

结论

综上所述,我们的结果表明,熊果苷可能有助于治疗 LPS 刺激引起的 BV2 小胶质细胞激活的炎症和有害影响。

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