Lee Jongsung, Jung Eunsun, Park Junho, Jung Kwangseon, Lee Sangyeop, Hong Sungtaek, Park Jinil, Park Eunkyung, Kim Jieun, Park Sanghee, Park Deokhoon
Biospectrum Life Science Institute, Yongin-city, Kyunggi-do, Korea.
Planta Med. 2005 Apr;71(4):338-43. doi: 10.1055/s-2005-864100.
Propionibacterium acnes, an anaerobic pathogen, plays an important role in the pathogenesis of acne and seems to initiate the inflammatory process by producing proinflammatory cytokines. In order to demonstrate the anti-inflammatory effects and action mechanisms of magnolol and honokiol, several methods were employed. Through DPPH and SOD activity assays, we found that although both magnolol and honokiol have antioxidant activities, honokiol has relatively stronger antioxidant activities than magnolol {[for DPPH assay, % of DPPH bleaching of magnolol and honokiol (500 microM magnolol: 19.8%; 500 microM honokiol: 67.3%)]; [for SOD assay, SOD activity (200 microM magnolol: 53.4%; 200 microM honokiol: 64.3%)]}. Moreover, the production of interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) induced by P. acnes in THP-1 cells, a human monocytic cell line, was reduced by magnolol and honokiol {[for IL-8 (10 microM magnolol: 42.7% inhibition; 10 microM honokiol: 51.4% inhibition)]; [for TNF-alpha (10 microM magnolol: 20.3% inhibition; 10 microM honokiol: 39.0% inhibition)]}. Cyclooxygenase-2 (Cox-2) activity was also suppressed by them [(15 microM magnolol: 45.8% inhibition), (15 microM honokiol: 66.3% inhibition)]. Using a nuclear factor-kappaB (NF-kappaB) luciferase reporter assay system and Western analysis, we identified that magnolol and honokiol exert their anti-inflammatory effects by inhibiting the NF-kappaB element, which exists in Cox-2, IL-8, and TNF-alpha promoters [(15 microM magnolol: 44.8% inhibition), (15 microM honokiol: 42.3% inhibition)]. Of particular note is that magnolol and honokiol operate downstream of the MEKK-1 molecule. Together with their previously known antibacterial activity against P. acnes and based on these results, we suggest that magnolol and honokiol may be introduced as possible acne-mitigating agents.
痤疮丙酸杆菌是一种厌氧病原体，在痤疮发病机制中起重要作用，似乎通过产生促炎细胞因子引发炎症过程。为了证明厚朴酚和和厚朴酚的抗炎作用及其作用机制，我们采用了几种方法。通过DPPH和超氧化物歧化酶（SOD）活性测定，我们发现虽然厚朴酚和和厚朴酚都具有抗氧化活性，但和厚朴酚的抗氧化活性相对强于厚朴酚{[DPPH测定，厚朴酚和和厚朴酚的DPPH脱色率（500微摩尔厚朴酚：19.8%；500微摩尔和厚朴酚：67.3%）]；[SOD测定，SOD活性（200微摩尔厚朴酚：53.4%；（200微摩尔和厚朴酚：64.3%）]}。此外，在人单核细胞系THP-1细胞中，痤疮丙酸杆菌诱导产生的白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）的量被厚朴酚和和厚朴酚减少{[IL-8（10微摩尔厚朴酚：抑制42.7%；10微摩尔和厚朴酚：抑制51.4%）]；[TNF-α（10微摩尔厚朴酚：抑制20.3%；10微摩尔和厚朴酚：抑制39.0%）]}。环氧合酶-2（Cox-2）活性也被它们抑制[（15微摩尔厚朴酚：抑制45.8%），（15微摩尔和厚朴酚：抑制66.3%）]。使用核因子-κB（NF-κB）荧光素酶报告基因检测系统和蛋白质免疫印迹分析，我们确定厚朴酚和和厚朴酚通过抑制存在于Cox-2、IL-8和TNF-α启动子中的NF-κB元件发挥其抗炎作用[（15微摩尔厚朴酚：抑制44.8%），（15微摩尔和厚朴酚：抑制42.3%）]。特别值得注意的是，厚朴酚和和厚朴酚在MEKK-1分子的下游发挥作用。结合它们先前已知的对痤疮丙酸杆菌的抗菌活性以及基于这些结果，我们认为厚朴酚和和厚朴酚可能作为可能的减轻痤疮药物被引入。
