Shiratsuchi Akiko, Ichiki Manami, Okamoto Yasuo, Ueda Natsuo, Sugimoto Naotoshi, Takuwa Yoh, Nakanishi Yoshinobu
Graduate School of Natural Science and Technology; Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan.
J Biochem. 2009 Jan;145(1):43-50. doi: 10.1093/jb/mvn139. Epub 2008 Oct 30.
The production of N-acylethanolamine (NAE) is enhanced during inflammation. NAE is synthesized from phosphatidylethanolamine with N-acylphosphatidylethanolamine (NAPE) as a precursor. The amount of NAPE at the site of inflammation exceeds that of NAE. This evokes the possibility that NAPE possesses a biological function, as does NAE. We here examined if N-palmitoylphosphatidylethanolamine (NPPE), a precursor of N-palmitoylethanolamine, modulates the state of inflammation. We found that the level of the phagocytosis of latex beads, Staphylococcus aureus, Escherichia coli, or apoptotic cells by mouse peritoneal macrophages or J774A.1 macrophages was reduced in the presence of liposomes containing NPPE, while that of dextran remained unaffected. This action of NPPE seemed to be due to the inhibition of the activation of Rac1 and Cdc42 in macrophages. These results suggested that NAPE is bioactive lipid acting toward the termination of inflammation.
在炎症过程中，N-酰基乙醇胺（NAE）的生成会增加。NAE由磷脂酰乙醇胺以N-酰基磷脂酰乙醇胺（NAPE）作为前体合成。炎症部位的NAPE量超过NAE。这引发了一种可能性，即NAPE与NAE一样具有生物学功能。我们在此研究了N-棕榈酰磷脂酰乙醇胺（NPPE），一种N-棕榈酰乙醇胺的前体，是否调节炎症状态。我们发现，在含有NPPE的脂质体存在的情况下，小鼠腹腔巨噬细胞或J774A.1巨噬细胞对乳胶珠、金黄色葡萄球菌、大肠杆菌或凋亡细胞的吞噬水平降低，而葡聚糖的吞噬水平不受影响。NPPE的这种作用似乎是由于抑制了巨噬细胞中Rac1和Cdc42的激活。这些结果表明，NAPE是一种对炎症终止起作用的生物活性脂质。
