Zhang Jie, Fang Huan, Zhang Jinguo, Guan Wencai, Xu Guoxiong
Department of Clinical Nutrition, Jinshan Hospital, Fudan University, Shanghai, China.
Department of Clinical Pharmacy, Jinshan Hospital, Fudan University, Shanghai, China.
Dose Response. 2020 May 19;18(2):1559325820926732. doi: 10.1177/1559325820926732. eCollection 2020 Apr-Jun.
Garcinol is a plant-derived compound that has some physiological benefits to human cells. However, the effect of garcinol on ovarian cancer (OC) cell proliferation and apoptosis is unknown. The current study aimed to examine the effects of garcinol alone and in combination with cisplatin (DDP) on cellular behavior and to explore the expression pattern of PI3K/AKT and nuclear factor-κB (NF-κB) in human OC cells. We found that OVCAR-3 cell viability was decreased after garcinol treatment. Garcinol alone and in combination with DDP significantly inhibited cell proliferation and had a synergistic effect evaluated by CompuSyn software. The cell cycle analysis showed the S phase arrest by garcinol. Furthermore, garcinol alone and in combination with DDP promoted cell apoptosis. The garcinol-induced apoptosis was further confirmed by the detection of cleavage forms of PARP and caspase 3. An increase in proapoptotic factor Bax expression was also found in garcinol-treated cells. Moreover, garcinol significantly decreased the phosphorylation of PI3K and AKT proteins and downregulated the expression of NF-κB. Thus, our data demonstrated that garcinol has the potential to be used as an anticancer agent and may synergize the effect of DDP. These actions are most likely through the regulation of the PI3K/AKT and NF-κB pathways.
藤黄脂是一种源自植物的化合物，对人体细胞具有一定的生理益处。然而，藤黄脂对卵巢癌（OC）细胞增殖和凋亡的影响尚不清楚。本研究旨在考察藤黄脂单独及与顺铂（DDP）联合使用对细胞行为的影响，并探究人OC细胞中PI3K/AKT和核因子-κB（NF-κB）的表达模式。我们发现，藤黄脂处理后OVCAR-3细胞活力下降。藤黄脂单独及与DDP联合使用均显著抑制细胞增殖，且通过CompuSyn软件评估具有协同作用。细胞周期分析显示藤黄脂使细胞停滞于S期。此外，藤黄脂单独及与DDP联合使用均促进细胞凋亡。通过检测PARP和caspase 3的裂解形式进一步证实了藤黄脂诱导的凋亡。在藤黄脂处理的细胞中还发现促凋亡因子Bax表达增加。此外，藤黄脂显著降低PI3K和AKT蛋白的磷酸化水平，并下调NF-κB的表达。因此，我们的数据表明藤黄脂有潜力用作抗癌药物，且可能增强DDP的疗效。这些作用很可能是通过调节PI3K/AKT和NF-κB信号通路实现的。
