摘要
目的:观察苦参碱在体内和体外的抗肿瘤作用。方法:MTT法检测苦参碱对小鼠腹水瘤细胞H2 2 的体外杀伤作用;AnnexinV -FITC/PI双标记法检测苦参碱对体外培养的H2 2 细胞的诱导凋亡作用;在BALB/C小鼠H2 2 移植瘤模型上观察苦参碱的体内抑瘤活性,透射电镜观察苦参碱治疗后荷瘤小鼠肝癌细胞的超微结构改变;免疫组化法检测荷瘤小鼠肝癌组织中Bcl- 2、Bax蛋白表达。结果:苦参碱在体外能够明显抑制H2 2 细胞的生长和增殖,并可诱导细胞凋亡;对小鼠肿瘤生长也有明显抑制作用,高、低浓度组抑瘤率分别为6 0 .71%和6 2 .5 3% ;用药组小鼠肿瘤组织中,电镜下可见较为典型的细胞凋亡的形态学改变;肿瘤组织中Bcl- 2蛋白表达明显降低,Bax蛋白表达增强,与荷瘤对照组相比有显著性差异(P <0 .0 1)。结论:苦参碱在体内外对H2 2 肿瘤细胞生长均有抑制作用,同时可促进肿瘤细胞表达Bax蛋白,抑制Bcl- 2表达,诱导肿瘤细胞凋亡。
Objective:To study the anti-tumor effects of matrine on murine hepatocarcinoma cell line H 22 in vitro and in vivo .Methods:Cytotoxicity effect of matrine on cultured H 22 cells was determined by MTT assay in vitro .Apoptosis of cultured H 22 cells induced by matrine were determined with Annexiin V-FITC/PI affinity assay.Tumor-bearing BALB/C mice were used to observe the inhibitory effects of matrine on H 22 cells in vivo .The ultra micro-structured changes of H 22 cells were observed by transmission electron microscope in tumor-bearing BALB/C mice after treated with matrine.The expressions of Bcl-2 & Bax protein were detected by immunohistochemical technique and the staining densities of Bcl-2 & Bax protein were quantitated through computerized image processing.The data were analyzed with one-way ANOVA by means of SPSS 10.0.Results:Matrine could obviously inhibit the growth and induce the apoptosis of cultured H 22 cells.Matrine also had significant anti-tumor activity,on mice bearing H 22 hepatoma.The inhibitory rates were above 60.7% and 62.5% in higher and lower doses groups,respectively ( P <0.01).Electron microscopy indicated the apoptosis of tumor cells with marginal nuclei,chromatin condensation and nuclei fragmentation,and apoptotic bodies were observed.The expression of Bcl-2 protein was down-regulated while that of Bax protein was up-regulated in tumor tissue treated with matrine.( P <0.01).Conclusion:Matrine has marked inhibitory effects on mice H 22 hepatoma cells both in vitro and in vivo .It can increase the expression of protein Bax and decrease expression of Bcl-2 to induce apoptosis of H 22 cells.
出处
《重庆医科大学学报》
CAS
CSCD
2005年第2期178-182,共5页
Journal of Chongqing Medical University
基金
国家自然科学基金 (3 0 17115 0 )