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红景天苷通过下调MAPK/NF-κB信号通路减弱LPS刺激的THP-1细胞来源巨噬细胞的活化。

Salidroside attenuates LPS-stimulated activation of THP-1 cell-derived macrophages through down-regulation of MAPK/NF-kB signaling pathways.

作者信息

Wang Hong-Wu, Wu Ting, Qi Jun-Ying, Wang Ya-Qi, Luo Xiao-Ping, Ning Qin

机构信息

Department of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2013 Aug;33(4):463-469. doi: 10.1007/s11596-013-1143-6. Epub 2013 Aug 1.

DOI:10.1007/s11596-013-1143-6
PMID:23904362
Abstract

Excessive activation of macrophages is implicated in various inflammatory injuries. Salidroside (Sal), one of the main bioactive components of Rhodiola Sachalinensis, has been reported to possess anti-inflammatory activities. This study aimed to examine the effect of Sal on the activation of macrophages and the possible mechanism. The lipopolysaccharide (LPS)-stimulated phrobol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophage models were established. The changes in the inflammatory profiles of THP-1-derived macrophages were determined. The results showed that Sal significantly decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), interleukin-1beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) at both mRNA and protein levels in THP-1-derived macrophages, and the effect was dose-depedent. Moreover, NF-κB activation was significantly suppressed and the phosphorylation of ERK, p38 and JNK was substantially down-regulated after Sal treatment. The findings suggested that Sal can suppress the activation of LPS-stimulated PMA-differetiated THP-1 cells, as evidenced by the decreased expression of iNOS, COX2, IL-1β, IL-6 and TNF-α, and the mechanism involves the inhibition of NF-κB activation and the phosphorylation of the MAPK signal pathway.

摘要

巨噬细胞的过度激活与多种炎症性损伤有关。红景天苷(Sal)是高山红景天的主要生物活性成分之一,据报道具有抗炎活性。本研究旨在探讨红景天苷对巨噬细胞激活的影响及其可能的机制。建立了脂多糖(LPS)刺激佛波酯12 - 肉豆蔻酸酯13 - 乙酸酯(PMA)分化的THP - 1巨噬细胞模型。测定了THP - 1来源巨噬细胞炎症谱的变化。结果表明,红景天苷在mRNA和蛋白水平上均显著降低了THP - 1来源巨噬细胞中诱导型一氧化氮合酶(iNOS)、环氧化酶 - 2(COX2)、白细胞介素 - 1β(IL - 1β)、白细胞介素 - 6(IL - 6)和肿瘤坏死因子 - α(TNF - α)的表达,且该作用呈剂量依赖性。此外,红景天苷处理后,NF - κB的激活受到显著抑制,ERK、p38和JNK的磷酸化水平大幅下调。这些发现表明,红景天苷可以抑制LPS刺激的PMA分化的THP - 1细胞的激活,iNOS、COX2、IL - 1β、IL - 6和TNF - α表达的降低证明了这一点,其机制涉及抑制NF - κB的激活和MAPK信号通路的磷酸化。

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