Choi Hyuk-Joon, Kang Ok-Hwa, Park Pil-Sang, Chae Hee-Sung, Oh Yoo-Chang, Lee Young-Seob, Choi Jang-Gi, Lee Go-Hoon, Kweon Oh-Hyun, Kwon Dong-Yeul
Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
J Med Food. 2007 Sep;10(3):460-6. doi: 10.1089/jmf.2006.198.
Mume Fructus (Family Rosaceae) is used as a traditional drug and health food in Asian countries. However, its therapeutic mechanisms and effects on macrophage-mediated inflammation remain unknown. In this study we examined the effect of Mume Fructus water extract (MFWE) on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The investigation focused on whether MFWE inhibited nitric oxide (NO) and prostaglandin (PG) E2 productions, as well as the expressions of inducible NO synthase (iNOS), cyclooxygenase (COX)-2, interleukin (IL)-6, nuclear factor-kappaB (NF-kappaB), and mitogen-activated protein kinases (MAPKs) in LPS-stimulated RAW 264.7 cells. We found that MFWE inhibited LPS-induced NO, PGE(2), and IL-6 productions as well as the expressions of iNOS and COX-2. Furthermore, MFWE suppressed the LPS-induced phosphorylations of p38 MAPK and extracellular signal-regulated kinase MAPK, as well as IkappaBalpha degradation and NF-kappaB activation. These results suggest that MFWE has inhibitory effects on LPS-induced PGE2, NO, and IL-6 production, as well as the expressions of iNOS and COX-2 in the murine macrophage. These inhibitory effects occur through blockades on the phosphorylation of MAPKs following IkappaBalpha degradation and NF-kappaB activation.
乌梅(蔷薇科)在亚洲国家被用作传统药物和保健食品。然而,其治疗机制以及对巨噬细胞介导的炎症的影响尚不清楚。在本研究中,我们检测了乌梅水提取物(MFWE)对脂多糖(LPS)刺激的RAW 264.7细胞中促炎介质的影响。研究重点在于MFWE是否抑制一氧化氮(NO)和前列腺素(PG)E2的产生,以及LPS刺激的RAW 264.7细胞中诱导型NO合酶(iNOS)、环氧化酶(COX)-2、白细胞介素(IL)-6、核因子-κB(NF-κB)和丝裂原活化蛋白激酶(MAPKs)的表达。我们发现MFWE抑制LPS诱导的NO、PGE2和IL-6的产生以及iNOS和COX-2的表达。此外,MFWE抑制LPS诱导的p38 MAPK和细胞外信号调节激酶MAPK的磷酸化,以及IκBα降解和NF-κB激活。这些结果表明,MFWE对LPS诱导的PGE2、NO和IL-6的产生以及小鼠巨噬细胞中iNOS和COX-2的表达具有抑制作用。这些抑制作用是通过在IκBα降解和NF-κB激活后阻断MAPKs的磷酸化而发生的。