Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju, Korea.
J Med Food. 2012 Jan;15(1):44-50. doi: 10.1089/jmf.2010.1540. Epub 2011 Nov 14.
The methanol extract of Codium fragile (MECF) has been reported to possess bioactive properties such as antidegranulation in eosinophils, as well as anti-edema, antibacterial, and antiviral activities. However, little is known about the molecular effects of MECF on lipopolysaccharide (LPS)-induced inflammation. Therefore, we investigated whether MECF affects the expression of inflammatory mediators in LPS-stimulated RAW 264.7 cells. To evaluate the anti-inflammatory effects of MECF, the cells were pretreated with MECF for 1 hour and then cultured with LPS for 24 hours. Our results indicate that MECF significantly attenuated secretion of LPS-induced inflammatory mediators nitric oxide (NO), prostaglandin E(2) (PGE(2)), and tumor necrosis factor (TNF)-α in RAW 264.7 cells. Additionally, LPS-induced mRNA and protein expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2, and TNF-α was decreased by pretreatment with MECF. These data indicate that MECF attenuates the expression of these inflammatory mediators at the transcriptional level. Therefore, we also investigated the effects of MECF on nuclear factor-κB (NF-κB) activity, which may be an important transcriptional factor for regulating the expression of iNOS, COX-2, and TNF-α mRNA. Our results showed that MECF reduced LPS-induced NF-κB activity via the suppression of nuclear translocation of the p50 and p65 NF-κB subunits and degradation of inhibitor of κB. In conclusion, we propose that MECF treatment down-regulates the expression and secretion of LPS-induced inflammatory mediators by inhibiting NF-κB activity.
脆江蓠甲醇提取物（MECF）已被报道具有生物活性，如抗嗜酸性粒细胞脱颗粒，以及抗水肿、抗菌和抗病毒活性。然而，对于 MECF 对脂多糖（LPS）诱导的炎症的分子作用知之甚少。因此，我们研究了 MECF 是否影响 LPS 刺激的 RAW 264.7 细胞中炎症介质的表达。为了评估 MECF 的抗炎作用，细胞先用 MECF 预处理 1 小时，然后用 LPS 培养 24 小时。结果表明，MECF 显著减弱了 LPS 诱导的 RAW 264.7 细胞中一氧化氮（NO）、前列腺素 E2（PGE2）和肿瘤坏死因子（TNF）-α的分泌。此外，MECF 预处理还降低了 LPS 诱导的诱导型一氧化氮合酶（iNOS）、环氧化酶（COX）-2 和 TNF-α的 mRNA 和蛋白表达。这些数据表明，MECF 在转录水平上减弱了这些炎症介质的表达。因此，我们还研究了 MECF 对核因子-κB（NF-κB）活性的影响，NF-κB 可能是调节 iNOS、COX-2 和 TNF-α mRNA 表达的重要转录因子。结果表明，MECF 通过抑制 p50 和 p65 NF-κB 亚基的核易位和 IκB 的降解来减少 LPS 诱导的 NF-κB 活性。总之，我们提出 MECF 通过抑制 NF-κB 活性来下调 LPS 诱导的炎症介质的表达和分泌。
