Molecular Nutrition Laboratory, Department of Food Science and Nutrition, Pukyong National University, 599-1 Daeyeon-3-dong, Nam-gu, Busan 608-737, South Korea.
Inflammation. 2013 Apr;36(2):259-71. doi: 10.1007/s10753-012-9542-6.
Microglial activation has been implicated in many neurological disorders for its inflammatory and neurotrophic effects. In this study, we investigated the effects of phlorofucofuroeckol A isolated from Ecklonia stolonifera Okamura on the production of inflammatory mediators in lipopolysaccharide (LPS)-stimulated microglia. Pre-treatment of phlorofucofuroeckol A attenuated the productions of nitric oxide, prostaglandin E2, and pro-inflammatory cytokines in LPS-stimulated microglia. Profoundly, phlorofucofuroeckol A treatment showed inactivation of nuclear factor-κB (NF-κB) by preventing the degradation of inhibitor κB-α and the nuclear translocation of p65 NF-κB subunit. Moreover, phlorofucofuroeckol A inhibited the activation of c-Jun NH2-terminal kinases (JNKs), p38 mitogen-activated protein kinase (MAPK), and Akt, but not that of extracellular signal-regulated kinase. These results indicate that phlorofucofuroeckol A inhibits the LPS-induced expression of inflammatory mediators through inactivation of NF-κB, JNKs, p38 MAPK, and Akt pathways. These findings suggest that phlorofucofuroeckol A can be considered as a nutraceutical candidate for the treatment of neuroinflammation in neurodegenerative diseases.
小胶质细胞激活因其炎症和神经营养作用而与许多神经退行性疾病有关。在这项研究中，我们研究了从裙带菜中分离得到的岩藻福酚 A 对脂多糖（LPS）刺激的小胶质细胞中炎症介质产生的影响。岩藻福酚 A 的预处理可减轻 LPS 刺激的小胶质细胞中一氧化氮、前列腺素 E2 和促炎细胞因子的产生。重要的是，岩藻福酚 A 通过阻止 IκB-α的降解和 p65 NF-κB 亚基的核易位来抑制核因子-κB（NF-κB）的失活。此外，岩藻福酚 A 抑制 c-Jun NH2-末端激酶（JNKs）、p38 丝裂原活化蛋白激酶（p38 MAPK）和 Akt 的激活，但不抑制细胞外信号调节激酶的激活。这些结果表明，岩藻福酚 A 通过抑制 NF-κB、JNKs、p38 MAPK 和 Akt 通路抑制 LPS 诱导的炎症介质表达。这些发现表明，岩藻福酚 A 可用作神经退行性疾病中神经炎症治疗的营养候选物。
