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枸杞水提物对脂多糖刺激的 RAW264.7 巨噬细胞的抗炎作用。

Anti-inflammatory effect of Lycium Fruit water extract in lipopolysaccharide-stimulated RAW 264.7 macrophage cells.

机构信息

Traditional Korean Medicine-TKM-Based Herbal Drug Research Group, Korea Institute of Oriental Medicine, 461-24 Jeonmin-dong, Yuseong, Daejeon 305-811, Republic of Korea.

出版信息

Int Immunopharmacol. 2012 Jun;13(2):181-9. doi: 10.1016/j.intimp.2012.03.020. Epub 2012 Apr 4.

DOI:10.1016/j.intimp.2012.03.020
PMID:22483979
Abstract

Lycium Fruit has been used as a traditional drug for low back pain and chronic cough in east-Asian countries. However, inhibitory effects of Lycium Fruit water extract (LFWE) on inflammation remain unknown. In this study, we investigated the inhibitory effects of LFWE on pro-inflammatory mediator production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. LFWE inhibited LPS-induced nitric oxide (NO), prostaglandin (PG) E₂, tumor necrosis factor (TNF)-α and interleukin (IL)-6 production as well as their synthesizing enzyme inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 gene expression. Furthermore, LFWE inhibited phosphorylations of extracellular signal-regulated kinase (ERK), p38 and c-Jun NH₂-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs) as well as suppression of IκBα degradation and nuclear translocation of nuclear factor (NF)-κB upon LPS stimulation. In addition, LFWE suppressed NO, PGE₂, TNF-α and IL-6 production in LPS-stimulated peritoneal macrophage cells. Taken together, our results suggest that LFWE inhibits the production of various inflammatory mediators via blockade on the MAPKs and NF-κB pathways. This finding first explains the mechanism of anti-inflammatory effect by LFWE in LPS-stimulated macrophage cells.

摘要

枸杞已被用作东亚国家治疗腰痛和慢性咳嗽的传统药物。然而,枸杞水提取物(LFWE)对炎症的抑制作用尚不清楚。在这项研究中,我们研究了 LFWE 对脂多糖(LPS)刺激的 RAW 264.7 细胞中促炎介质产生的抑制作用。LFWE 抑制 LPS 诱导的一氧化氮(NO)、前列腺素(PG)E₂、肿瘤坏死因子(TNF)-α 和白细胞介素(IL)-6 的产生,以及诱导型一氧化氮合酶(iNOS)和环氧化酶(COX)-2 基因表达的合成酶。此外,LFWE 抑制 LPS 刺激后细胞外信号调节激酶(ERK)、p38 和 c-Jun NH₂-末端激酶(JNK)丝裂原激活蛋白激酶(MAPKs)的磷酸化以及 IκBα 降解和核因子(NF)-κB 的核易位。此外,LFWE 抑制 LPS 刺激的腹腔巨噬细胞中 NO、PGE₂、TNF-α 和 IL-6 的产生。总之,我们的研究结果表明,LFWE 通过阻断 MAPKs 和 NF-κB 通路抑制各种炎症介质的产生。这一发现首次解释了 LFWE 在 LPS 刺激的巨噬细胞中抗炎作用的机制。

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