Jeju Biodiversity Research Institute, Jeju High-Tech Development Institute, Jeju, Republic of Korea.
Food Chem Toxicol. 2010 May;48(5):1222-9. doi: 10.1016/j.fct.2010.02.014. Epub 2010 Feb 13.
In the present study, the chemical constituents of Artemisia fukudo essential oil (AFE) were investigated using GC-MS. The major constituents were alpha-thujone (48.28%), beta-thujone (12.69%), camphor (6.95%) and caryophyllene (6.01%). We also examined the effects of AFE on the production of nitric oxide (NO), prostaglandin E(2) (PGE(2)), tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6, in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. Western blotting and RT-PCR tests indicated that AFE has potent dose-dependent inhibitory effects on pro-inflammatory cytokines and mediators. We investigated the mechanism by which AFE inhibits NO and PGE(2) by examining the level of nuclear factor-kappaB (NF-kappaB) activation within the mitogen-activated protein kinase (MAPK) pathway, which is an inflammation-induced signal pathway in RAW 264.7 cells. AFE inhibited LPS-induced ERK, JNK, and p38 phosphorylation. Furthermore, AFE inhibited the LPS-induced phosphorylation and degradation of Ikappa-B-alpha, which is required for the nuclear translocations of the p50 and p65 NF-kappaB subunits in RAW 264.7 cells. Our results suggest that AFE might exert an anti-inflammatory effect by inhibiting the expression of pro-inflammatory cytokines. Such an effect is mediated by a blocking of NF-kappaB activation which consequently inhibits the generation of inflammatory mediators in RAW264.7 cells. AFE may be useful for treating inflammatory diseases.
在本研究中，使用 GC-MS 研究了艾蒿精油（AFE）的化学成分。主要成分是α-侧柏酮（48.28％），β-侧柏酮（12.69％），樟脑（6.95％）和石竹烯（6.01％）。我们还研究了 AFE 对脂多糖（LPS）激活的 RAW 264.7 巨噬细胞中一氧化氮（NO），前列腺素 E2（PGE2），肿瘤坏死因子（TNF）-α，白细胞介素（IL）-1β和 IL-6产生的影响。 -1β和 IL-6。 Western blotting 和 RT-PCR 测试表明，AFE 对促炎细胞因子和介质具有强大的剂量依赖性抑制作用。我们通过检查丝裂原激活的蛋白激酶（MAPK）途径中核因子-κB（NF-κB）激活的水平来研究 AFE 抑制 NO 和 PGE2 的机制，这是 RAW 264.7 细胞中炎症诱导的信号途径。 AFE 抑制 LPS 诱导的 ERK，JNK 和 p38 磷酸化。此外，AFE 抑制了 Ikappa-B-alpha 的 LPS 诱导的磷酸化和降解，这是 RAW 264.7 细胞中 p50 和 p65 NF-κB 亚基核易位所必需的。我们的结果表明，AFE 可能通过抑制促炎细胞因子的表达发挥抗炎作用。这种作用是通过阻断 NF-κB 激活来介导的，从而抑制了 RAW264.7 细胞中炎症介质的产生。 AFE 可能对治疗炎症性疾病有用。
