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[灵菌红素作用机制的药理学分析]

[Pharmacological analysis of the mechanism of action of prodigiozan].

作者信息

Alekhin E K, Kalimullina D Kh

出版信息

Antibiotiki. 1983 Jun;28(6):442-5.

PMID:6309077
Abstract

It was shown experimentally on mice that prodigiozan did not increase the acute toxicity of prednisolone. It lowered the prednisolone-induced reduction of the period of hexenal sleep and preserved the capacity for increasing resistance to infection, when the adrenal cortex was blocked with metopiron. These findings together with the literature data were interpreted as arguments against the assumption that glucocorticoid mobilization was an important factor of the prodigiozan mode of action. Blocking of the beta-adrenoreceptors with obsidan increased the capacity of prodigiozan to activate the macrophage system and to raise the nonspecific resistance to infection, while blocking of the alpha-adrenoreceptors with phenolphthalein lowered this capacity. It was suggested that the macrophage activation was mediated by the alpha-adrenoreceptors and was due to a decrease in the cAMP/cGMP ratio.

摘要

在小鼠身上进行的实验表明,灵菌红素不会增加泼尼松龙的急性毒性。当用甲吡酮阻断肾上腺皮质时,它能减轻泼尼松龙诱导的己烯醛睡眠时间缩短,并保留增强抗感染能力。这些发现与文献数据一起被解释为反对糖皮质激素动员是灵菌红素作用模式的重要因素这一假设的论据。用奥布西旦阻断β-肾上腺素能受体会增加灵菌红素激活巨噬细胞系统和提高非特异性抗感染能力,而用酚酞阻断α-肾上腺素能受体则会降低这种能力。有人认为巨噬细胞的激活是由α-肾上腺素能受体介导的,并且是由于环磷酸腺苷/环磷酸鸟苷比值降低所致。

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