Hayashi Y, Hirai S, Negishi M, Okumura T, Ichikawa A
Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
Biochem Pharmacol. 1991 Jun 1;41(11):1725-30. doi: 10.1016/0006-2952(91)90176-6.
The effects of glycyrrhizin and its aglycone, glycyrrhetinic acid, on the cytoplasmic free calcium concentration ([Ca2+]i) in mastocytoma P-815 cells, DNP-Ascaris (antigen) sensitized mast cells, hepatocytes, fibroblasts and endothelial cells were investigated. In these cell types, glycyrrhetinic acid in the concentration range of 20 to 100 microM caused an increase in [Ca2+]i and inhibited calcium increases induced by an antigen (mast cells), ATP, phenylephrine (hepatocytes) and thrombin (fibroblasts and endothelial cells). Stimulation with phenylephrine, in place of glycyrrhetinic acid, did not inhibit subsequent calcium increases induced by phenylephrine or ATP. On the other hand, glycyrrhizin at concentrations up to 100 microM neither caused an increase in [Ca2+]i nor inhibited calcium increases induced by other stimulatory substances. These results suggest that the inhibition of the calcium-mediated signal pathway may participate in the cytostatic actions of glycyrrhetinic acid.
研究了甘草酸及其苷元甘草次酸对肥大细胞瘤P - 815细胞、二硝基苯 - 蛔虫（抗原）致敏肥大细胞、肝细胞、成纤维细胞和内皮细胞胞质游离钙浓度（[Ca2+]i）的影响。在这些细胞类型中，浓度范围为20至100微摩尔的甘草次酸会导致[Ca2+]i升高，并抑制由抗原（肥大细胞）、ATP、去氧肾上腺素（肝细胞）和凝血酶（成纤维细胞和内皮细胞）诱导的钙升高。用去氧肾上腺素代替甘草次酸进行刺激，并不会抑制随后由去氧肾上腺素或ATP诱导的钙升高。另一方面，浓度高达100微摩尔的甘草酸既不会导致[Ca2+]i升高，也不会抑制由其他刺激物质诱导的钙升高。这些结果表明，抑制钙介导的信号通路可能参与了甘草次酸的细胞生长抑制作用。
