Anti-inflammatory Effect of Euphorbiae kansui Radix Extract in Lipopolysaccharide-stimulated M ouse Peritoneal Macrophages

Jeung-beum Kim, H. Kyung, H. Kang
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Abstract

This study is aimed to investigate the anti-inflammatory effect of Euphorbiae kansui radix methanol extract (ERE) in lipopolysaccharide(LPS)-stimulated mouse peritoneal macrophages. Peritoneal macrophages were obtained from thioglycollate-injected Balb/c mice. Cells were stimulated with LPS or LPS plus interferon-gamma (IFN-γ) in the presence of ERE and various inflammatory markers were assayed. Finally, LPS-induced signaling molecules were measured. ERE up to 400 ㎍/㎖, was not cytotoxic to ERE inhibited LPS/IFN-γ-induced nitric oxide (NO), inducible NO synthase. ERE also reduced the levels of cyclooxygenase-2 and the proinflammatory cytokines such as tumor necrosis factor-α, interleukin(IL)-6 and IL-12. The inhibitory effect of ERE on LPS-induced IκBα degradation was weak but phosphorylation of JNK, p38 and ERK1/2 was strongly suppressed. Our data indicated that the anti-inflammatory effect of ERE in LPS-stimulated macrophages was partly mediated by its inhibition of JNK, p38 and ERK1/2.
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宽水大戟提取物对脂多糖刺激小鼠腹腔巨噬细胞的抗炎作用
本研究旨在探讨大戟甲醇提取物(ERE)对脂多糖(LPS)刺激小鼠腹腔巨噬细胞的抗炎作用。从注射巯基乙酸酯的Balb/c小鼠中获得腹腔巨噬细胞。在ERE存在的情况下,用LPS或LPS加干扰素γ (IFN-γ)刺激细胞,并检测各种炎症标志物。最后,测量lps诱导的信号分子。ERE≤400毫升,对细胞无毒害,ERE抑制LPS/IFN-γ诱导的一氧化氮(NO)、诱导的NO合成酶。ERE还降低了环氧化酶-2和促炎细胞因子如肿瘤坏死因子-α、白细胞介素(IL)-6和IL-12的水平。ERE对lps诱导的i - κ b α降解的抑制作用较弱,但JNK、p38和ERK1/2的磷酸化被强烈抑制。我们的数据表明,在lps刺激的巨噬细胞中,ERE的抗炎作用部分是通过抑制JNK、p38和ERK1/2介导的。
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