Gao Chao, Li Xuehua, Yu Shuangshuang, Liang Liang
Department of Hepatobiliary Surgery, Liaocheng People's Hospital, Dongchangfu District, Liaocheng, Shandong 252000, China.
J BUON. 2019 Sep-Oct;24(5):1964-1969.
Liver cancer accounts for considerable mortality across the globe. The sharp upsurge in the incidence of liver cancer, unavailability of standard treatments and the adverse side effects associated with the existing drugs has made it compulsory to explore novel and more effective anticancer molecules. In this study the anticancer effects of a natural compound oleanolic acid were investigated in vitro.
The human HepG2 liver cancer cells were treated with various concentrations of oleanolic acid for 24 h. The antiproliferative effects of oleanolic acid were measured by CCK8 cell viability assay. DAPI and annexin V/propidium iodide (PI) assays were employed to examine the induction of apoptosis. Transwell assay was performed to examine the cell migration and invasion. Expression analysis was performed by western blot analysis.
The results showed that oleanolic acid decreased the viability of the liver cancer HepG2 cells and exhibited an IC50 of 30 µM. The cytotoxicity of oleanolic acid was also investigated on the normal liver cells AML12 and it was found that oleanolic acid and exerted very low toxic effects on these cells and exhibited an IC50 of 120 µM. Oleanolic acid also caused remarkable changes in the morphology of the HepG2 cells and inhibited their colony formation potential. Flow cytometry indicated oleanolic acid triggered G2/M arrest of the liver HepG2 cancer cells. PI and DAPI staining revealed that oleanolic acid prompted apoptosis of the HepG2 cells. The apoptotic cells increased from 2.2% in control to around 35% at 30 µM concentration. Oleanolic acid also suppressed the migration and invasion of the liver cancer cells via blocking of the JNK/p38 signalling pathway.
The results of the current research revealed that oleanolic acid can be a molecule that may be utilised in the treatment of liver cancer in the future.
肝癌在全球范围内导致相当高的死亡率。肝癌发病率的急剧上升、标准治疗方法的缺乏以及现有药物的不良副作用，使得探索新型且更有效的抗癌分子成为必然。在本研究中，对天然化合物齐墩果酸的抗癌作用进行了体外研究。
用不同浓度的齐墩果酸处理人肝癌HepG2细胞24小时。通过CCK8细胞活力测定法测量齐墩果酸的抗增殖作用。采用DAPI和膜联蛋白V/碘化丙啶（PI）测定法检测细胞凋亡的诱导情况。进行Transwell测定以检测细胞迁移和侵袭。通过蛋白质印迹分析进行表达分析。
结果表明，齐墩果酸降低了肝癌HepG2细胞的活力，IC50为30μM。还研究了齐墩果酸对正常肝细胞AML12的细胞毒性，发现齐墩果酸对这些细胞的毒性非常低，IC50为120μM。齐墩果酸还引起了HepG2细胞形态的显著变化，并抑制了它们的集落形成潜力。流式细胞术表明齐墩果酸触发了肝癌HepG2细胞的G2/M期阻滞。PI和DAPI染色显示齐墩果酸促使HepG2细胞凋亡。凋亡细胞从对照组的2.2%增加到30μM浓度时的约35%。齐墩果酸还通过阻断JNK/p38信号通路抑制肝癌细胞的迁移和侵袭。
当前研究结果表明，齐墩果酸可能是一种未来可用于治疗肝癌的分子。
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