熟地黄多糖对H22荷瘤小鼠细胞色素C和Caspase-3蛋白的影响

Effect of RPS on Cytochrome C and Caspase- 3 Protein in Hepatoma H22- Bearing Mice

目的:探讨熟地黄多糖对H22荷瘤小鼠线粒体凋亡途径中细胞色素C和Caspase-3的作用机制。方法:用H22肝癌腹水瘤株接种小鼠右侧腋下构建实体瘤模型,随机分组为模型组、环磷酰胺组、熟地黄多糖组,连续灌胃给药8 d。剥离肿瘤组织,应用免疫组化法分别检测肿瘤组织中细胞色素C与Caspase-3的表达情况。结果:熟地黄多糖可使H22瘤小鼠肿瘤组织中细胞色素C和Caspase-3的表达水平明显增高,与模型组比较差异显著(P<0.01)。结论:熟地黄多糖能上调H22荷瘤小鼠肿瘤内细胞色素C和Caspase-3的表达,其机制可能是促进线粒体释放细胞色素C及其Caspase-3的激活,启动线粒体凋亡途径,从而诱导肿瘤细胞凋亡来发挥抗肿瘤作用。

Objective： To investigate the mechanism of cell apoptosis via mitochondria pathway induced by Radix Rehmanniae polysaccharides（ RPS） in H22 tumor- bearing mice. The target spots were Cytochrome C and Caspase- 3.Methods： After establishing H22 tumor- bearing mice models,we grouped them randomly into a model group,a cyclophosphamide group and a RPS group. Eight days later,the tumor tissue was stripped and we tested the expression of Cytochrome C and Caspase- 3 by IHC. Results： RPS could increase the levels of Cytochrome C and Caspase- 3 of H22 tumor tissue compared with the control group（ P 0. 01）. Conclusion： RPS can upregulate the expressions of Cytochrome C and Caspase- 3 of H22 tumor tissue. We suppose RPS can play a key role in stimulating release of Cytochrome C and Caspase- 3 from mitochondrion and induce cell apoptosis via mitochondria pathway,which will induce tumor cell apoptosis. RPS has an anti- tumor effect through the mechanism.