甲基丙烯酰紫草素的抗肿瘤作用及其机制的研究

Antitumor effect and mechanism of methyl-acrylshikonin

目的研究甲基丙烯酰紫草素(MA)在体内外的抗肿瘤作用,并探讨其作用机制。方法用MTT法和生长曲线法研究不同浓度的MA对SGC-7901细胞的生长抑制作用;应用S180荷瘤小鼠模型进行其体内抗瘤实验;免疫组化法检测凋亡相关蛋白NF-κB p50的表达。结果MA对SGC-7901细胞具有抑制作用,且呈明显的量效和时效关系,其IC50=14.12±1.83mg.L-1;0.375、0.750、1.500 mg.kg-1的MA对小鼠移植性肉瘤S180的抑制率分别为25.00%、41.20%、61.11%,呈剂量依赖性;随着MA浓度的增大,NF-κB p50蛋白的表达下调。结论MA具有较好的体内外抗肿瘤作用,可能与诱导细胞凋亡和抑制NF-κB p50的活性有关。

OBJECTIVE To explore in vitro and in vivo antitumor effects of methyl - acrylshikonin （MA） and the mechanisms. METHODS MTT assay and growth curve assay were used to assess the inhibitory effect of MA on the proliferation of SGC -7901 cells; S180 sarcoma model in mice was applied to study antitumor effect of MA in vivo; Apoptosis associated protein NF - KB p50 was detected by immunohistochemistry. RESULTS MTT assay showed MA could inhibit the proliferation of SGC - 7901 cells, and IC50 of MA to SGC -7901 cells was 14.12 ± 1.83 mg·L^-1. The dose - effect relation and time - effect relation were described in growth curve. Under the treatment of 0. 375,0.75,1.5 mg·kg^-1 of MA,the inhibitory rates of S180 xenograft tumor in mice were 25.00%, 41.20% and 61.11%, respectively. Immunohistochemistry revealed MA could inhibit the NF - KB p50 in a concentration - dependent manner. CONCLUSION Methyl - acrylshikonin has in vivo and in vitro antitumor effects which are related to induced cell apoptosis and inhibited NF - kB p50 activity in tumor.