Asperlin From the Marine-Derived Fungus Aspergillus sp SF-5044 Exerts Anti-inflammatory Effects Through Heme Oxygenase-1 Expression in Murine Macrophages
Asperlin From the Marine-Derived Fungus Aspergillus sp SF-5044 Exerts Anti-inflammatory Effects Through Heme Oxygenase-1 Expression in Murine Macrophages
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DOI：
10.1254/jphs.10219fp
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发表时间：
2011-07-01
影响因子：
3.5
通讯作者：
Kim, Youn-Chul
中科院分区：
文献类型：
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作者：
Lee, Dong-Sung;Jeong, Gil-Saeng;Kim, Youn-Chul
Asperlin 是从曲霉属 (Aspergillus sp.) 中分离出来的真菌代谢产物。 SF-5044。在本研究中，我们从海洋来源的真菌曲霉属中分离出了阿斯珀林。 SF-5044 并证明它在脂多糖 (LPS) 刺激的 RAW264.7 和小鼠腹膜巨噬细胞中抑制诱导型一氧化氮合酶 (iNOS) 表达，减少 iNOS 衍生的 NO，抑制环氧合酶 (COX)-2 表达，并减少 COX 衍生的前列腺素 (PG) E-2 产生。同样，阿培林减少了肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-1 β 的产生。此外，asperlin还能抑制RAW264.7巨噬细胞中I kappa B-α的磷酸化和降解，以及LPS刺激引起的p65核转位。此外，asperlin 通过核因子 E2 相关因子 2 的核转位诱导血红素加氧酶 (HO)-1 表达，并增加 RAW264.7 巨噬细胞中的 HO 活性。 asperlin 对 LPS 诱导的 iNOS 和 COX-2 表达以及 NO、PGE(2)、TNF-α 和 IL-1 beta 产生的影响可被 HO-1 抑制剂锡原卟啉部分逆转。这些发现表明，asperlin 诱导的 HO-1 表达在 asperlin 在巨噬细胞中的抗炎作用中发挥作用。
Asperlin is a fungal metabolite isolated from Aspergillus sp. SF-5044. In the present study, we isolated asperlin from the marine-derived fungus Aspergillus sp. SF-5044 and demonstrated that it inhibited inducible nitric oxide synthase (iNOS) expression, reduced iNOS-derived NO, suppressed cyclooxygenase (COX)-2 expression, and reduced COX-derived prostaglandin (PG) E-2 production in lipopolysaccharide (LPS)-stimulated RAW264.7 and murine peritoneal macrophages. Similarly, asperlin reduced the production of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta. In addition, asperlin inhibited the phosphorylation and degradation of I kappa B-alpha, as well as the nuclear translocation of p65 caused by the stimulation of LPS in RAW264.7 macrophages. Furthermore, asperlin induced heme oxygenase (HO)-1 expression through nuclear translocation of nuclear factor E2 related factor 2 and increased HO activity in RAW264.7 macrophages. The effects of asperlin on the LPS-induced expression of iNOS and COX-2 and production of NO, PGE(2), TNF-alpha, and IL-1 beta were partially reversed by a HO-1 inhibitor, tin protoporphyrin. These findings suggest that asperlin-induced HO-1 expression plays a role in the anti-inflammatory effects of asperlin in macrophages.