Lloret S, Moreno J J
Departamento de Ciencias Fisiológicas, Unidad de Fisiología, Fac. Farmacia, Univ. Barcelona, Spain
Int J Biochem Cell Biol. 1996 Apr;28(4):465-72. doi: 10.1016/1357-2725(95)00149-2.
The present study investigated the role of kinases and G-proteins in arachidonic acid (AA) mobilization by resident mouse peritoneal macrophages in response to phagocytosis of opsonized zymosan. Stimulation of resident murine peritoneal macrophages with opsonized zymosan caused an increase in [3H] arachidonic acid release. This increase was dose-dependent and was not accompanied by de novo synthesis of proteins. Neither staurosporine, a protein kinase C inhibitor, nor genistein, a tyrosine kinase inhibitor, had any effect on [3H] AA mobilization, although trifluoperazine significantly inhibited AA release. The involvement of G proteins and phospholipase C (PLC) in the regulation of arachidonic acid release induced by opsonized zymosan was also examined in mouse peritoneal macrophages. Prior treatment of cells with pertussis toxin induced a partial decrease in AA mobilization. However, neomycin or aspirin, at doses that inhibit inositol phosphate formation (PLC activity), did not [3H] AA mobilization by PLA2. We proposed that the AA release by peritoneal macrophages in response to opsonized zymosan phagocytosis could be due to the participation of enzymes other than PLC and PKC, or proteins other than G proteins.
本研究调查了激酶和G蛋白在驻留小鼠腹腔巨噬细胞吞噬调理酵母聚糖后花生四烯酸（AA）动员过程中的作用。用调理酵母聚糖刺激驻留小鼠腹腔巨噬细胞会导致[3H]花生四烯酸释放增加。这种增加呈剂量依赖性，且不伴有蛋白质的从头合成。蛋白激酶C抑制剂星形孢菌素和酪氨酸激酶抑制剂染料木黄酮对[3H] AA动员均无任何影响，尽管三氟拉嗪能显著抑制AA释放。还在小鼠腹腔巨噬细胞中研究了G蛋白和磷脂酶C（PLC）在调理酵母聚糖诱导的花生四烯酸释放调节中的作用。用百日咳毒素预先处理细胞会导致AA动员部分减少。然而，新霉素或阿司匹林在抑制肌醇磷酸形成（PLC活性）的剂量下，对PLA2介导的[3H] AA动员没有影响。我们推测，腹腔巨噬细胞对调理酵母聚糖吞噬的反应中AA释放可能是由于PLC和PKC以外的酶或G蛋白以外的蛋白质的参与。
