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目的 通过丹参酮 I(tanshinone I)对肿瘤细胞的体内外实验研究 ,探讨丹参酮 I抗肿瘤作用及作用机制。方法 人肝癌细胞 (Hep G2 )培养液中加入不同浓度的丹参酮 I,培养 72小时 ,观察 Hep G2细胞的增殖率 ;倒置显微镜下观察 Hep G2细胞的形态变化 ;流式细胞仪 (FCM)检测 Hep G2细胞周期及凋亡率 ;免疫组化检测 Hep G2细胞的增殖凋亡调控相关基因 (Bax、Bcl- 2 )的蛋白表达。用 Hep G2细胞制作 Balb/c裸鼠荷瘤模型 ,每天腹腔注射丹参酮 I1次连续 10天 ,观察抑瘤率。结果 丹参酮 I抑制 Hep G2细胞生长 ;阻滞 Hep G2细胞周期于 G0 /G1 期并诱导细胞凋亡 ;通过下调 Bcl- 2基因表达 (P<0 .0 1) ,上调 Bax基因表达 (P<0 .0 1)诱导 Hep G2细胞凋亡 ;抑制荷瘤裸鼠肿瘤生长 ,抑瘤率为 33.3%。结论 丹参酮 I具有抗肿瘤活性 ,其作用机制之一是诱导细胞凋亡。
Objective To study the antitumor effect and mechanism of tanshinone I on tumor cells in vitro and in vivo by tanshinone I. Methods Different concentrations of tanshinone I were added into Hep G2 culture medium and cultured for 72 hours to observe the proliferation rate of Hep G2 cells. The morphological changes of Hep G2 cells were observed under inverted microscope. The apoptosis of Hep G2 cells was detected by flow cytometry (FCM) G2 cell cycle and apoptosis rate. The protein expression of Bax and Bcl-2 in Hep G2 cells was detected by immunohistochemistry. Balb / c nude mice bearing tumor model was made by Hep G2 cells. Tanshinone I was injected intraperitoneally for 10 consecutive days for 10 days to observe the tumor inhibition rate. Results Tanshinone I could inhibit the growth of Hep G2 cells, block the Hep G2 cell cycle in G0 / G1 phase and induce apoptosis. Upregulate Bax gene expression by down-regulating Bcl-2 gene expression (P <0.01) .0 1) induced Hep G2 cell apoptosis; inhibited tumor growth in tumor-bearing nude mice, with a tumor inhibition rate of 33.3%. Conclusion Tanshinone I has anti-tumor activity, and its mechanism of action is to induce apoptosis.