Evans A T, Sharma P, Ryves W J, Evans F J
Department of Pharmacognosy, School of Pharmacy, London, UK.
FEBS Lett. 1990 Jul 16;267(2):253-6. doi: 10.1016/0014-5793(90)80938-f.
The non-tumour promoting irritant, resiniferatoxin, was capable of activating the NADPH-oxidase respiratory burst of starch-elicited, but not resident mouse peritoneal macrophages in vitro. Unlike TPA, the response was synergised by incubation with zymosan. The Rx-stimulated NADPH-oxidase activity in a cell-free assay was selectively enhanced in the presence of exogenous Rx-kinase rather than PKC and in the absence of Ca2+. Since resiniferatoxin is a poor activator of PKC, it is probable that the Ca2(+)-independent Rx-kinase plays a role in activation of the macrophage respiratory burst following stimulation by zymosan.
非促肿瘤刺激物树脂毒素能够在体外激活淀粉诱导的小鼠腹腔巨噬细胞的NADPH氧化酶呼吸爆发，但不能激活常驻巨噬细胞。与佛波酯不同，与酵母聚糖共同孵育可增强该反应。在无细胞试验中，外源性树脂毒素激酶而非蛋白激酶C存在且无Ca2+时，树脂毒素刺激的NADPH氧化酶活性会选择性增强。由于树脂毒素是蛋白激酶C的弱激活剂，Ca2+非依赖性树脂毒素激酶可能在酵母聚糖刺激后巨噬细胞呼吸爆发的激活中发挥作用。
