胶红酵母CICC 33013胞外多糖抑制肝癌细胞活性研究

Inhibitory effect of exo-polysaccharide from Rhodotorula mucilaginosa CICC 33013 on hepatocellular carcinoma cell activity

采用四甲基偶氮唑蓝(MTT)法对胶红酵母胞外多糖组分(Rhodotorula mucilaginosa exo-polysaccharide2-A,REPS2-A)抑制10种常见癌细胞(血癌细胞K562、胃癌细胞BGC823、胃癌细胞SGC7901、胃癌细胞MKN28、肝癌细胞HepG2、BEL7402、Hep3B、胰腺癌细胞HS66T、乳腺癌细胞SKBR3、宫颈癌细胞HeLa)能力进行了筛选,结果证明胞外多糖组分REPS2-A对肝癌细胞HepG2有较好的抑制效果。通过胞外多糖组分REPS2-A对HepG2细胞抑制作用最佳浓度及时效性的研究,探讨胞外多糖组分REPS2-A对肝癌HepG2细胞的生长抑制及其作用机制。结果表明:当胞外多糖组分REPS2-A的浓度为1mg/mL时,肝癌细胞HepG2的抑制率高于IC50时的抑制率,抑制效果明显优于其他浓度。肝癌细胞HepG2的自发凋亡率为0.40%,当胞外多糖组分REPS2-A浓度为1mg/mL,分别处理24,48,72h,肝癌细胞HepG2的凋亡率依次为77.70%,88.18%,97.08%。胞外多糖组分REPS2-A能有效抑制肝癌细胞的增殖,使肝癌细胞HepG2阻滞发生在G1/S期,并诱导肝癌细胞HepG2凋亡,且存在剂量效应。

The anti-tumor activity of the exo-polysaccharide component REPS2-A metabolized by Rhodotorula mucilaginosa CICC33013 was studied.The exo-polysaccharide component REPS2-A was inhibited by tetramethylazole blue(MTT)method in 10 common cancer cells including blood cancer cell K562,gastric cancer cell BGC823,gastric cancer cell SGC7901,gastric cancer cell MKN28,liver cancer cell HepG2,BEL7402,Hep3 B,pancreatic cancer cell HS66 T,breast cancer cell SKBR3,and cervical cancer cell HeLa.The results showed that the exo-polysaccharide component REPS2-A had a good inhibitory effect on HepG2 cells.By studying the optimal concentration and time effect of exo-polysaccharide component REPS2-A on HepG2 cells,the growth inhibition and its mechanism of exo-polysaccharide component REPS2-A on HepG2 cells were investigated.The results showed that when the concentration of exo-polysaccharide component REPS2-A was 1 mg/mL,the inhibition rate of HepG2 in liver cancer cells was higher than that in IC50,and the inhibition effect was significantly better than that in other concentrations.The spontaneous apoptosis rate of HepG2 was 0.40%.When the concentration of exo-polysaccharide component REPS2-A was1 mg/mL,the apoptosis rate of HepG2 was 77.70%,88.18%and 97.08% after 24,48 and 72 htreatment,respectively.Exopolysaccharide component REPS2-A could effectively inhibit the proliferation of liver cancer cells,cause HepG2 block in the G1/S phase,and induce HepG2 apoptosis in liver cancer cells with dose effect.