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目的研究长梗秦艽酮体外抗肿瘤活性,探讨其部分作用机制。方法采用噻唑蓝(MTT)法观察长梗秦艽酮对BEL-7402,HeLa,BXPC-3,PANC-1细胞增殖的影响,流式细胞术分析其对BEL-7402细胞周期的影响,Western blot法检测其对ERK1/2蛋白激酶磷酸化的作用,RT-PCR法检测其对p53和乙酰肝素酶(heparanase)的mRNA表达水平的影响。结果长梗秦艽酮能够显著抑制4种肿瘤细胞的生长。长梗秦艽酮作用于BEL-7402细胞后能够引起S期细胞周期阻滞,激活ERK1/2磷酸化而对p38磷酸化没有影响,上调p53的mRNA表达水平,抑制乙酰肝素酶的mRNA表达。结论长梗秦艽酮具有显著的抗肿瘤活性,其作用机制可能与激活ERK1/2信号通路及上调p53基因从而诱导细胞周期阻滞和抑制乙酰肝素酶的表达有关。
Aim To study the anti-tumor activity of long-stemmed Gentiiridin in vitro and its mechanism of action. Methods MTT method was used to observe the effects of long-term Qin Qin ketone on the proliferation of BEL-7402, HeLa, BXPC-3 and PANC-1 cells. Flow cytometry was used to analyze the cell cycle of BEL-7402 cells. Western blot The phosphorylation of ERK1 / 2 protein kinase was detected by RT-PCR. The effect of p53 on the mRNA expression of p53 and heparanase was detected by RT-PCR. Results Long Qin Qin ketone can significantly inhibit the growth of four kinds of tumor cells. Long-acting genistein could induce cell cycle arrest in S phase and activate ERK1 / 2 phosphorylation, but had no effect on p38 phosphorylation, upregulate p53 mRNA expression and inhibit heparanase mRNA expression in BEL-7402 cells. CONCLUSION Long-acting genistein has significant antitumor activity. Its mechanism may be related to the activation of ERK1 / 2 signaling pathway and the upregulation of p53 gene to induce cell cycle arrest and inhibition of heparanase expression.