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目的:研究三白草提取物(extracts from Saururi Herba,ESH)的抗乳腺癌转移作用。方法:采用尾静脉注射肿瘤细胞法建立实验性转移模型;采用体外细胞黏附、迁移以及侵袭法,观察ESH对乳腺癌细胞系MDA-MB-231细胞的体外黏附、迁移以及侵袭的影响;采用Runx2转录因子分析法和Western blot法,观察ESH对Runx2活性的影响。结果:给药后,ESH 200,400 mg·kg-1剂量组裸鼠肺组织中人ck19的平均表达量分别为55.85%,42.28%,显著低于空白组(P<0.01);体外黏附实验表明,ESH可干扰肿瘤细胞与细胞外基质蛋白之间的黏附(P<0.01);ESH 80,160 g·L-1剂量组的细胞迁移细胞数分别为(106.4±52.4),(40.4±7.6)个,与空白组相比具有统计学差异(P<0.01);细胞侵袭实验表明,ESH低、中、高剂量组的侵袭细胞抑制率分别为32.57%,68.04%和71.92%,与空白组相比具有统计学差异(P<0.01)。Runx2转录因子活性分析以及Western blot实验结果表明,ESH可显著抑制Runx2的磷酸化,从而抑制其转录活性。结论:ESH具有明显的抗乳腺癌转移作用。抑制细胞内Runx2磷酸化可能是其发挥抗转移作用的机制之一。
OBJECTIVE: To study the anti breast metastatic effect of extracts from Saururi Herba (ESH). Methods: Tumor cells were injected into tail vein to establish experimental metastasis model. The adhesion, migration and invasion of breast cancer cell line MDA-MB-231 cells were observed by cell adhesion, migration and invasion in vitro. Runx2 Transcription factor analysis and Western blot were used to observe the effect of ESH on Runx2 activity. Results: After administration, the average expression of human ck19 in the lung tissue of ESH treated with 200 and 400 mg · kg -1 ESH was 55.85% and 42.28%, respectively, which was significantly lower than that of the blank group (P <0.01). In vitro adhesion experiments showed that, ESH could interfere with the adhesion between tumor cells and extracellular matrix proteins (P <0.01). The number of migrating cells in the groups of ESH 80,160 g · L-1 were (106.4 ± 52.4) and (40.4 ± 7.6) (P <0.01). The cell invasion assay showed that the inhibitory rates of invasive cells in ESH low, medium and high dose groups were 32.57%, 68.04% and 71.92%, respectively, which were statistically significant compared with the blank group Learning difference (P <0.01). Runx2 transcription factor activity analysis and Western blot results show that, ESH can significantly inhibit Runx2 phosphorylation, thereby inhibiting its transcriptional activity. Conclusion: ESH has a significant anti-metastatic effect on breast cancer. Inhibition of intracellular Runx2 phosphorylation may be its anti-metastasis mechanism.