Standardized Material Bank for New Botanical Drugs, College of Pharmacy, Wonkwang University, Iksan, Republic of Korea; College of Pharmacy, Wonkwang University, Iksan 570-749, Republic of Korea.
Eur J Pharmacol. 2013 Dec 5;721(1-3):267-76. doi: 10.1016/j.ejphar.2013.09.026. Epub 2013 Sep 27.
The root of Polygala tenuifolia Willd. (Polygalaceae) is well known for its use in the treatment of neurasthenia, amnesia, and inflammation. In this study, we isolated phenyl propanoid type metabolite tenuifoliside A, one of the phenylpropanoids from P. tenuifolia, and investigated its anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW264.7 and murine peritoneal macrophages. The results showed that tenuifoliside A inhibited the production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PG E2), and cyclooxygenase (COX)-2. In addition, tenuifoliside A suppressed the production of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. We also evaluated the effects of tenuifoliside A on the activation of nuclear factor-kappaB (NF-κB). Tenuifoliside A inhibited the translocation of the NF-κB subunit p65 into the nucleus by interrupting the phosphorylation and degradation of inhibitor kappa B (IκB)-α in LPS-stimulated murine peritoneal macrophages. Moreover, we confirmed that the suppression of the inflammatory process by tenuifoliside A was mediated through the mitogen-activated protein kinases (MAPKs) pathway based on the fact that tenuifoliside A significantly decreased p-c-Jun N-terminal kinase (p-JNK) protein expression in LPS-stimulated murine peritoneal macrophages. Taken together, the anti-inflammatory effects of tenuifoliside A were mediated by the inhibition of the NF-κB and MAPK pathways. This study is the first report on the anti-inflammatory effects of tenuifoliside A, and the strong anti-inflammatory effects of tenuifoliside A provide potential compound to be developed as therapeutic for inflammatory diseases.
远志根（远志科）因治疗神经衰弱、健忘和炎症而广为人知。在这项研究中，我们从远志中分离出苯丙素类代谢产物远志糖苷 A，并研究了其对脂多糖（LPS）刺激的 RAW264.7 细胞和小鼠腹腔巨噬细胞的抗炎作用。结果表明，远志糖苷 A 抑制了一氧化氮（NO）、诱导型一氧化氮合酶（iNOS）、前列腺素 E2（PGE2）和环氧化酶（COX）-2 的产生。此外，远志糖苷 A 还抑制了促炎细胞因子如肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β的产生。我们还评估了远志糖苷 A 对核因子-κB（NF-κB）激活的影响。远志糖苷 A 通过中断 LPS 刺激的小鼠腹腔巨噬细胞中 IκB-α的磷酸化和降解，抑制 NF-κB 亚基 p65 向核内易位。此外，我们证实，基于远志糖苷 A 显著降低 LPS 刺激的小鼠腹腔巨噬细胞中 p-c-Jun N-末端激酶（p-JNK）蛋白表达的事实，远志糖苷 A 通过抑制丝裂原活化蛋白激酶（MAPKs）途径来抑制炎症过程。综上所述，远志糖苷 A 的抗炎作用是通过抑制 NF-κB 和 MAPK 途径介导的。这项研究首次报道了远志糖苷 A 的抗炎作用，其强烈的抗炎作用为开发治疗炎症性疾病的潜在化合物提供了依据。
