Kwon Dong-Joo, Bae Young-Soo, Ju Sung Mi, Youn Gi Soo, Choi Soo Young, Park Jinseu
Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702; Hongcheon Institute of Medicinal Herb, Hongcheon 200-930, Korea.
Department of Forest Biomaterials Engineering, Kangwon National University, Chuncheon 200-701, Korea.
BMB Rep. 2014 Jun;47(6):318-23. doi: 10.5483/bmbrep.2014.47.6.200.
We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-κB activation, such as IKK activation, IκBα phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-κB and JNK MAPK signaling cascades in macrophages.
我们从欧美杨树皮提取物中分离出酚类糖苷水杨苷，并使用脂多糖（LPS）刺激的RAW264.7细胞研究了其抑制炎症反应的能力以及这些能力背后的分子机制。水杨苷在LPS刺激的RAW 264.7细胞中以剂量依赖性方式抑制诱导型一氧化氮合酶（iNOS）表达及随后的一氧化氮（NO）生成。水杨苷显著抑制LPS诱导的RAW 264.7细胞中核因子κB（NF-κB）激活的信号级联反应，如IκB激酶（IKK）激活、IκBα磷酸化和p65磷酸化。此外，水杨苷抑制LPS诱导的应激活化蛋白激酶（JNK）激活，但不抑制细胞外信号调节激酶（ERK）或p38丝裂原活化蛋白激酶（p38 MAPK）。此外，水杨苷显著抑制LPS刺激的RAW 264.7细胞中促炎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）的产生。这些发现表明，水杨苷可能通过抑制巨噬细胞中NF-κB和JNK丝裂原活化蛋白激酶信号级联反应来抑制LPS诱导的促炎介质表达，从而发挥其抗炎活性。
