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Cryptotanshinone Suppressed Inflammatory Cytokines Secretion in RAW264.7 Macrophages through Inhibition of the NF-κB and MAPK Signaling Pathways

机译:隐丹参酮通过抑制NF-κB和MAPK信号通路抑制RAW264.7巨噬细胞中炎性细胞因子的分泌

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摘要

Cryptotanshinone (CTS), a major constituent extracted from the medicinal herb Salvia miltiorrhiza Bunge, has well-documented antioxidative and anti-inflammatory effects. In the present study, the pharmacological effects and underlying molecular mechanisms of CTS on lipopolysaccharide (LPS)-induced inflammatory responses were investigated. By enzyme-linked immunosorbent assay, we observed that CTS reduced significantly the production of proinflammatory mediators (tumor necrosis factor-α and interleukin-6) induced by LPS in murine macrophage-like RAW264.7 cells. Mechanistically, CTS inhibited markedly the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, p38MAPK, and JNK, which are crucially involved in regulation of proinflammatory mediator secretion. Moreover, immunofluorescence and western blot analysis indicated that CTS abolished completely LPS-triggered nuclear factor-κB (NF-κB) activation. Taken together, these data implied that NF-κB and MAPKs might be the potential molecular targets for clarifying the protective effects of CTS on LPS-induced inflammatory cytokine production in macrophages.
机译:隐丹参酮(CTS)是从药草丹参中提取的主要成分,具有良好的抗氧化和抗炎作用。在本研究中,研究了CTS对脂多糖(LPS)诱导的炎症反应的药理作用和潜在的分子机制。通过酶联免疫吸附测定,我们观察到CTS显着降低了LPS诱导的小鼠巨噬细胞样RAW264.7细胞中促炎性介质(肿瘤坏死因子-α和白介素6)的产生。从机制上讲,CTS显着抑制促分裂原激活的蛋白激酶(MAPK)的磷酸化,包括ERK1 / 2,p38MAPK和JNK,这与促炎性介质分泌的调节至关重要。此外,免疫荧光和蛋白质印迹分析表明CTS完全消除了LPS触发的核因子-κB(NF-κB)激活。综上所述,这些数据暗示NF-κB和MAPK可能是阐明CTS对LPS诱导的巨噬细胞炎症细胞因子产生的保护作用的潜在分子靶标。

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