Xanthomicrol, a trimethoxylated hydroxyflavone, is the main active component of Dracocephalum kotschyi Boiss leaf extract. Preliminary in vitro studies identified this compound as a potential antiangiogenic and anticancer agent. This study aimed to evaluate in vivo anticancer effect of xanthomicrol and investigate its molecular mechanism of action in a mouse melanoma (B16F10) model. Effect of xanthomicrol on B16F10 melanoma cell viability was determined using the MTT assay. For in vivo experiments, C57BL/6 mice were inoculated subcutaneously with B16F10 cells. After five days, once daily administration of xanthomicrol, thalidomide, or vehicle was commenced and continued for 21 consecutive days. On the 26th day, blood samples and tumor biopsies were taken for subsequent molecular analysis. Xanthomicrol showed inhibitory effect on viability of B16F10 melanoma cells (IC50 value: 3.433 μg/ml). Initial tumor growth, tumor volume and weight, and angiogenesis were significantly decreased in xanthomicrol-treated animals compared with those in vehicle group. Protein expression of phosphorylated Akt, mRNA expressions of HIF-1α and VEGF in tumor tissues, and serum VEGF were significantly decreased in xanthomicrol-treated animals compared with vehicle-treated animals. Thus, xanthomicrol inhibited cancer cell growth both in vitro and in vivo. This effect, at least in part, was exerted by interfering with PI3K/Akt signaling pathway and inhibiting VEGF secretion by tumor cells. Further studies are required to elucidate the exact molecular mechanisms of antitumor activity of xanthomicrol.

中文翻译：

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Xanthomicrol在小鼠黑素瘤（B16F10）同种异体移植模型中发挥抗血管生成和抗肿瘤作用

Xanthomicrol是一种三甲氧基化羟基黄酮，是Dracocephalum kotschyi的主要活性成分。博伊斯叶提取物。初步的体外研究确定该化合物为潜在的抗血管生成和抗癌剂。这项研究旨在评估xanthomicrol的体内抗癌作用，并研究其在小鼠黑素瘤（B16F10）模型中的分子作用机理。使用MTT测定法确定黄原胶对B16F10黑色素瘤细胞活力的影响。对于体内实验，用B16F10细胞皮下接种C57BL / 6小鼠。五天后，开始每天一次施用黄原胶，沙利度胺或赋形剂，并连续连续21天。在第26天，采集血样和肿瘤活检样品用于随后的分子分析。Xanthomicrol显示对B16F10黑素瘤细胞的活力的抑制作用（IC 50值：3.433  μ克/毫升）。与载体组相比，经黄原微处理的动物的初始肿瘤生长，肿瘤体积和重量以及血管生成显着降低。与媒介物处理的动物相比，黄原微处理的动物的磷酸化Akt的蛋白质表达，肿瘤组织中的HIF- 1α和VEGF的mRNA表达以及血清VEGF显着降低。因此，异黄酮在体外和体内均抑制癌细胞的生长。至少部分地通过干扰PI3K / Akt信号传导途径并抑制肿瘤细胞的VEGF分泌来发挥这种作用。需要进一步的研究以阐明抗黄粉蛋白抗肿瘤活性的确切分子机制。