玛卡多糖抗非小细胞肺癌作用及其机制

目的:探讨玛卡多糖抗非小细胞肺癌作用及其机制。方法:采用一定浓度的玛卡多糖处理非小细胞肺癌A549细胞,CCK-8法、划痕实验和Transwell小室检测玛卡多糖对A549细胞增殖、迁移和侵袭的影响;流式细胞术检测玛卡多糖对A549细胞周期和凋亡的影响;实时荧光定量PCR和Western Blot法检测细胞周期和凋亡相关因子的表达。结果:玛卡多糖能显著抑制A549细胞的增殖、迁移和侵袭;细胞周期被阻滞在G₀/G₁期和G₂/M期;实时荧光定量PCR结果显示,CDK-1和Cyclin B1的表达显著降低,Caspase-3、Caspase-8、Caspase-9的表达显著升高;Western Blot结果发现,周期相关蛋白CDK-1、Cyclin B1、CDK-4、CDK-6、Cyclin D1的表达显著降低,凋亡相关蛋白Caspase-3、Caspase-8、Caspase-9、Bax的表达显著升高,Bcl-2的表达显著降低。结论:玛卡多糖能够抑制非小细胞肺癌A549细胞的增殖并促进细胞凋亡。

Effects and mechanism of Maca polysaccharide on non-small cell lung cancer

OBJECTIVE To investigate the effects and mechanism of Maca polysaccharide on non-small cell lung cancer.METHODS Non-small cell lung cancer A549 cells were treated with Maca polysaccharide at a certain concentration, and the effects of Maca polysaccharide on the proliferation, migration and invasion of A549 cells were observed by CCK-8 scratch assay and transwell chamber. Flow cytometry was used to detect the effects of Maca polysaccharide on the cell cycle and apoptosis of A549 cells. The expression of cell cycle and apoptosis related factors were measured by real-time quantitative PCR and Western Blot.RESULTS Maca polysaccharides could significantly inhibit the proliferation, migration and invasion of A549 cells. The cell cycle was arrested in G₀/G₁ and G₂/M phases. Real-time quantitative PCR showed that the expression levels of CDK-1 and Cyclin B1 were significantly decreased, while the expression levels of Caspase-3, Caspase-8 and Caspase-9 were significantly increased. Western blot indicated that the expression of cyclin-related protein CDK-1, Cyclin B1, CDK-4, CDK-6 and Cyclin D1 were significantly down-regulated, while the expression of apoptosis-related proteins Caspase-3, Caspase-8, Caspase-9 and Bax were significantly up-regulated and Bcl-2 was significantly reduced.CONCLUSION Maca polysaccharides can inhibit the proliferation and promote the apoptosis of non-small cell lung cancer A549 cells.