板蓝根组酸诱导耐药人肝癌原位移植瘤的细胞凋亡研究

目的　研究板蓝根组酸诱导耐药人肝癌原位移植瘤的细胞凋亡作用及机制。方法　利用已建立的人耐药肝癌BEL 74 0 4 /ADM动物模型 ,应用FCM、透射电子显微镜等方法观察板蓝根组酸在体内对耐药肝癌细胞的形态学特征变化。结果　FCM检测到的凋亡细胞为 :BEL 74 0 4细胞组 0 5 % ,ADM组为 8 3% ,组酸 ADM组为 1 7 6 % ,两组比较有显著性差异 (P <0 0 5 ) ;电镜下见组酸 ADM组的肿瘤组织中多个凋亡细胞聚集 ,细胞核内染色质空虚 ,或染色质浓缩成新月体帽状结构 ,核仁浓缩或碎裂 ,凋亡小体形成 ,粗面内质网结构松散、脱粒、滑面内质网增多 ,排列无序 ,线粒体呈泡状或出现絮状物 ,嵴模糊不清 ,桥粒连接疏松 ,细胞膜微绒毛脱落或消失 ,溶酶体减少。结论　经组酸 ADM作用于肿瘤后 ,耐药肝癌中凋亡细胞明显增多 ,肝癌细胞的超微结构形态学改变符合程序化死亡的过程 ,说明板蓝根组酸联合ADM能诱导耐药肝癌细胞发生凋亡 ,具有逆转耐药作用。

The study of cell apoptosis in human drug-resistant orthotopic transplanted hepatocellular carcinoma induced bv Isatis tinctoria L combination acid

Obsjective To study the effect and mechanism of cell apoptosis in human drug resistant orthotopic transplanted hepatocellular carcinoma(HCC) induced by Isatis tinctoria L combination acid.Methods Flow cytometry(FCM) and electromicroscope were used to observed the morphological changes of drug resistant HCC cell expose to Isatis tinctoria L combination acid in BEL 7404/ADM(adriamycin) animal model.Results the rate of apoptotic cell was 0 5% in group BEL 7404,The rate of apoptotic cell was significantly lower in group ADM(8 3%) than in group combination acid and ADM(17 6%)(P<0 05).Under the observation of electromicroscope,the tumor tissue of group combination acid and ADM showed:many apoptotic cell aggregation,chromatin was hollow or chromatin condense to petal like structure,The nucleus pyknosis or karyorrhexis,apoptosis body formation,rough endoplastic reticula diffusion,slippy endoplastic reticula increased and out of order array,mitochondria became swelled and vacuolalized or produced flocculi,desmosome junctions loosened,microvilli fall off or disappeared,lysosomes decreased.Conclusion Apoptotic cell of drug resistant HCC were significantly increased after expose to combination acid and ADM.The changes of ultrastructure of HCC accord with the process of procedural cell death.It suggested Isatis tinctoria L combination acid and ADM could induced drug resistant HCC cell apoptosis and have the effect in reversing drug resistant.