论文部分内容阅读
目的通过体外体内实验探讨鸦胆子油脂质体对人肝癌细胞株HepG2的影响及可能机制。方法利用鸦胆子油脂质体高剂量(5mg/L)、低剂量(2.5mg/L)体外作用于人肝癌细胞株HepG2,MTT比色分析法分析HepG2细胞生长抑制程度,流式细胞仪检测不同药物浓度作用下细胞的凋亡率,透射电镜下观察HepG2细胞形态变化。通过腹腔注射荷瘤裸鼠进行体内试验,观察鸦胆子油脂质体小剂量(12.5mg/L)、大剂量(25mg/L)对其肝脏的病理改变;TUNEL法检测肝脏肿瘤组织凋亡细胞。结果 MTT比色分析法实验结果显示鸦胆子油脂质体可明显抑制HepG2细胞增殖;透射电镜下观察5mg/L鸦胆子油脂质体在体外作用于HepG2细胞6h后,可见明显凋亡细胞形态出现。流式细胞仪检测随鸦胆子油脂质体作用强度和时间的增加,细胞抑制率逐步由33.31%提升至90.62%(P<0.01)。鸦胆子油脂质体腹腔注射组较阴性对照组动物模型死亡时平均体重增加,肿瘤转移率下降(P<0.01);TUNEL法亦提示鸦胆子油脂质体组凋亡细胞率增加(P<0.01)。结论鸦胆子油脂质体对HepG2细胞在体内体外具有抑制增殖的作用,并可诱导肿瘤细胞凋亡。
Objective To investigate the effects of Brucea javanica liposomes on human hepatoma cell line HepG2 in vitro and its possible mechanism. Methods The human hepatocellular carcinoma HepG2 cells were treated with high dose (5mg / L) and low dose (2.5mg / L) of Brucea javanica oil. MTT colorimetric assay was used to analyze the growth inhibition of HepG2 cells. Flow cytometry was used to detect the effect of different drugs The apoptosis rate of HepG2 cells was observed under transmission electron microscope. The tumor-bearing nude mice were inoculated intraperitoneally to observe the pathological changes of Brucea javanica oil liposomes in small dose (12.5mg / L) and high dose (25mg / L), and TUNEL method was used to detect apoptotic cells in liver tumor. Results MTT colorimetric assay showed that Brucea javanica oil liposomes could significantly inhibit the proliferation of HepG2 cells. The morphological changes of HepG2 cells were observed after 5mg / L Brucea javanica liposomes treated with HepG2 cells for 6h in vitro. Flow cytometry with Brucea javanica oil plastid intensity and time increase, the cell inhibition rate gradually increased from 33.31% to 90.62% (P <0.01). The average body weight and tumor metastasis rate of Brucea javanica liposome group were significantly lower than those of the negative control group (P <0.01). TUNEL method also suggested that the apoptotic cell ratio of Brucea javanica oil liposome group increased (P <0.01) . Conclusion Brucea javanica liposomes can inhibit the proliferation of HepG2 cells in vitro and in vivo and induce tumor cell apoptosis.