Li Jinwei, Li Xiaodan, Cai Wenci, Liu Yuanfa
State Key Laboratory of Food Science and Technology, Synergetic Innovation Center of Food Safety and Nutrition, School of Food Science and Technology, Jiangnan University, Wuxi, 214122, P.R. China.
School of Food Science and Technology, Jiangnan University, 214122, Wuxi, Jiangsu Province, China.
Lipids Health Dis. 2016 Feb 16;15:30. doi: 10.1186/s12944-016-0201-z.
Total polar compounds (TPC) formed during successive frying have the negative healthy effects. However, little researches focused on the cytotoxicity of different parts of TPC. The present study was carried out to elucidate the different polar compounds-induced apoptosis in human hepatocellular carcinoma (HCC) HepG2 cells. The polar compounds of frying oil named oxidized triglycerides oligo (TGO), oxidized triglycerides dimer (TGD), and oxidize triglycerides (ox-TG) were isolated and collected via HPLC. MTT assay was selected to determine the cell viability, and apoptosis rate of the cells was analyzed with the help of flow cytometry. The results indicated that TGO, TGD, or ox-TG could suppress the proliferation of HepG2 cells and improve the cell apoptosis in the concentration- and time- dependent manner. Different polar compounds have the different activity of cytotoxicity and apoptosis (p < 0.05), and ox-TG was the most serious deleterious on HepG2 cell viability and apoptotic, followed by TGO and TGD. At the concentration of 2.00 mg/ml and incubated for 48 h, the cell inhibition rate and apoptotic rate of HepG2 induced by ox-TG could reach 23.0 % and 16.05 %, respectively. Cell cycle analysis showed that the inhibition of TGO, TGD, and ox-TG on HepG2 cells mainly occurred in S phase.
连续油炸过程中形成的总极性化合物(TPC)具有负面健康影响。然而,很少有研究关注TPC不同部分的细胞毒性。本研究旨在阐明不同极性化合物诱导人肝癌(HCC)HepG2细胞凋亡的情况。通过高效液相色谱法分离并收集了煎炸油中的极性化合物,即氧化甘油三酯低聚物(TGO)、氧化甘油三酯二聚体(TGD)和氧化甘油三酯(ox-TG)。选择MTT法测定细胞活力,并借助流式细胞术分析细胞凋亡率。结果表明,TGO、TGD或ox-TG能够以浓度和时间依赖性方式抑制HepG2细胞的增殖并促进细胞凋亡。不同极性化合物具有不同的细胞毒性和凋亡活性(p < 0.05),其中ox-TG对HepG2细胞活力和凋亡的损害最为严重,其次是TGO和TGD。在2.00 mg/ml浓度下孵育48小时,ox-TG诱导的HepG2细胞抑制率和凋亡率分别可达23.0%和16.05%。细胞周期分析表明,TGO、TGD和ox-TG对HepG2细胞的抑制主要发生在S期。