细胞培养生产的紫草色素与天然紫草色素理化性质比较

对细胞培养生产的紫草色素与天然紫草色素进行了理化性质比较研究，结果表明，两者的耐热性、耐氧化性及不同ｐＨ值条件下颜色的变化无明显差异，而耐还原性则具显著差异。此外，还对细胞培养生产的紫草色素和天然紫草色素的组成成份进行了ＴＬＣ和ＨＰＬＣ分析，发现两者组成成份基本一致，只是相对含量具一定差异．     

紫草中活性成分的体外抗癌作用

对紫草中化学成分进行了抗癌活性研究。以顺氯氨铂(DDP)为阳性对照,通过形态学、MTT实验考察了从紫草中分离得到的7个化合物对人胃癌细胞MGC-803和人肝癌细胞BEL-7402的增殖抑制作用,并以抑制率和半数抑制浓度(IC50)为指标进行了评价。结果表明,7个化合物在体外对两株癌细胞有不同程度的抑制作用。去氧紫草素(Ⅰ)、β,β-二甲基丙烯酰紫草素(Ⅱ)、异丁酰紫草素(Ⅲ)、紫草素(Ⅳ)、甲基紫草素(Ⅴ)、β-谷甾醇(Ⅵ)、咖啡酸脂肪醇酯混合物(Ⅶ)和DDP对胃癌细胞MGC-803的IC50分别为:1.7、1.4、7.0、0.5、1.5、>100、>100和4.4μg/mL;对肝癌细胞BEL-7402的IC50分别为:1.5、1.3、34.0、1.3、1.4、>100、>100和7.6μg/mL。证明从紫草分离得到的萘醌类化合物(Ⅰ-Ⅴ)对人胃癌细胞MGC-803和人肝癌细胞BEL-7402的生长有较强的抑制作用,呈明显的剂量-药效依赖关系,其中化合物Ⅰ、Ⅱ、Ⅳ、Ⅴ的抗肿瘤活性远强于阳性药物DDP。化合物Ⅵ、Ⅶ则没有抑制这两株癌细胞的作用。     

聚氨酯泡沫原位提取培养紫草细胞生产紫草色素

在紫草细胞培养过程中影响紫草色素进一步合成的重要因素之一是色素在细胞内大量积累，为促进紫草色素向胞外分泌，建立了一种新的培养体系，即以聚氨酯泡沫作为色素吸附介质，加入到细胞培养液中原位吸附提取培养紫草细胞生产紫草色素。结果表明：聚氨酯泡沫的加入明显促进紫草色素的合成及分泌，细胞合成的９５％（质量分数，下同）以上的色素被聚氨酯泡沫吸咐分离，同时也发现在培养早期（０４ｄ）加入适量的（９ｇ／Ｌ）聚氨酯泡沫可使色素产量提高３０８倍。采用丙酮和乙醇洗脱吸附的紫草色素具有优良的解吸效果。另外，试验还比较了原位提取培养体系与非原位提取培养体系细胞对蔗糖利用情况以及ｐＨ值变化情况。     

Shikonin Inhibits the Migration and Invasion of Human Glioblastoma Cells by Targeting Phosphorylated β-Catenin and Phosphorylated PI3K/Akt: A Potential Mechanism for the Anti-Glioma Efficacy of a Traditional Chinese Herbal Medicine

Shikonin is an anthraquinone derivative extracted from the root of lithospermum. Shikonin is traditionally used in the treatment of inflammatory and infectious diseases such as hepatitis. Shikonin also inhibits proliferation and induces apoptosis in various tumors. However, the effect of shikonin on gliomas has not been fully elucidated. In the present study, we aimed to investigate the effects of shikonin on the migration and invasion of human glioblastoma cells as well as the underlying mechanisms. U87 and U251 human glioblastoma cells were treated with shikonin at 2.5, 5, and 7.5 μmol/L and cell viability, migration and invasiveness were assessed with CCK8, scratch wound healing, in vitro Transwell migration, and invasion assays. The expression and activity of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) and the expression of phosphorylated β-catenin (p-β-catenin) and phosphorylated PI3K/Akt were also checked. Results showed that shikonin significantly inhibited the cell proliferation, migration, invasion, and expression of MMP-2 and MMP-9 in U87 and U251 cells. The expression of p-β-catenin showed contrary trends in two cell lines. It was significantly inhibited in U87 cells and promoted in U251 cells. Results in this work indicated that shikonin displayed an inhibitory effect on the migration and invasion of glioma cells by inhibiting the expression and activity of MMP-2 and -9. In addition, shikonin also inhibited the expression of p-PI3K and p-Akt to attenuate cell migration and invasion and MMP-2 and MMP-9 expression in both cell lines, which could be reversed by the PI3K/Akt pathway agonist, insulin-like growth factor-1 (IGF-1).