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首页> 外文期刊>European Journal of Medicinal Chemistry: Chimie Therapeutique >Ergosterol elicits oxidative burst in tobacco cells via phospholipase A_2 and protein kinase C signal pathway
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Ergosterol elicits oxidative burst in tobacco cells via phospholipase A_2 and protein kinase C signal pathway

机译：麦角固醇通过磷脂酶A_2和蛋白激酶C信号通路在烟草细胞中引起氧化性爆发

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摘要

Ergosterol, a typical fungal sterol, induced in tobacco (Nicotiana tabacum L. cv. Xanthi) suspension cells the synthesis of reactive oxygen species and alkalization of the external medium that are dependent on the mobilization of calcium from internal stores. We used specific inhibitors to elucidate the signal pathway triggered by ergosterol compared with cryptogein, a proteinaceous elicitor of Phytophthora cryptogea. Herbimycin A and genistein, inhibitors of tyrosine protein kinases, had no effect on the oxidative burst and pH changes induced by both elicitors. Similarly, H-89, an inhibitor of protein kinase A, had no effect on the induction of these defense reactions. However, the response to both elicitors was completely blocked by NPC-15437, a specific inhibitor of animal protein kinase C (PKC). The responses induced by cryptogein but not those induced by ergosterol were inhibited by U73122 and neomycin, inhibitors of phospholipase C (PLC). On the other hand, the activity of phospholipase A+2 (PLA+2) measured using a fluorogenic substrate was stimulated by ergosterol and not by cholesterol and cryptogein. A specific inhibitor of PLA+2, arachidonic acid trifluoromethyl ketone (AACOCF+3), inhibited the pathway stimulated by ergosterol but not that induced by cryptogein. These results suggest that the cryptogein-induced signal pathway leading to the oxidative burst and ΔpH changes includes PLC and PKC, whereas this response induced by ergosterol includes PLA+2 and PKC.
机译：麦角固醇是一种典型的真菌固醇，它在烟草（Nicotiana tabacum L. cv。Xanthi）悬浮细胞中诱导合成依赖于从内部存储中动员的钙的活性氧物种的合成和外部介质的碱化。与隐藻疫霉的蛋白质激发子隐藻毒素相比，我们使用了特定的抑制剂来阐明麦角固醇触发的信号通路。酪氨酸蛋白激酶抑制剂除草霉素A和染料木黄酮对两种引发剂引起的氧化爆发和pH变化均无影响。同样，蛋白激酶A的抑制剂H-89对这些防御反应的诱导也没有影响。但是，对这两个激发子的反应被NPC-15437（一种动物蛋白激酶C（PKC）的特异性抑制剂）完全阻断了。 U73122和磷脂酶C（PLC）的抑制剂新霉素抑制了隐菌素诱导的反应，但麦角固醇诱导的反应没有受到抑制。另一方面，使用荧光底物测得的磷脂酶A + 2（PLA + 2）的活性是由麦角固醇而不是胆固醇和隐血球蛋白刺激的。 PLA + 2的一种特异抑制剂花生四烯酸三氟甲基酮（AACOCF + 3）抑制了麦角固醇刺激的途径，但没有抑制隐血球蛋白诱导的途径。这些结果表明，隐伏蛋白诱导的导致氧化爆发和ΔpH变化的信号途径包括PLC和PKC，而麦角固醇诱导的这种反应包括PLA + 2和PKC。

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