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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。
Aim To study the apoptosis and its mechanism of isradia acid-induced apoptosis in orthotopic transplanted hepatocellular carcinoma. Methods The established human resistant hepatocellular carcinoma BEL7440 / ADM animal model was used to observe the morphological changes of the resistant Hepatoma cells in vivo by FCM and transmission electron microscopy. Results The number of apoptotic cells detected by FCM was 0 5% in BEL 74 0 4 cells group, 83% in ADM group and 176% in acid + ADM group, with significant difference between the two groups (P <0 0 5). Under the electron microscope, a number of apoptotic cells were found in the tumor tissue of the acid + ADM group, with chromatin vacuoles in the nucleus or chromatin condensed into crescent cap-like structures, condensed or fragmented nucleolus, and small apoptotic cells Body formation, rough endoplasmic reticulum structure loose, threshed, slip surface endoplasmic reticulum increased, disordered arrangement, the mitochondria bubble or floc, cristae blurred, bridge desmosome loose, cell membrane microvilli shed or disappeared , Lysosomes decreased. CONCLUSION: The apoptotic cells in drug-resistant hepatocellular carcinoma are significantly increased by the combination of acid and ADM, and the ultrastructural changes of liver cancer cells are in accordance with the process of programmed death, indicating that the combination of isradine and ADM can induce the development of drug- Apoptosis, with reversal of drug resistance.