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首页> 外文期刊>Life sciences >Tea polyphenols enhance cisplatin chemosensitivity in cervical cancer cells via induction of apoptosis
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Tea polyphenols enhance cisplatin chemosensitivity in cervical cancer cells via induction of apoptosis

机译：茶多酚通过诱导细胞凋亡增强顺铂对宫颈癌细胞的化学敏感性

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Aim Constitutive activation of nuclear factor-kappaB (NF-κB) and Akt has been implicated in chemoresistance as well as inhibition of apoptosis to cisplatin (CDDP), therefore, we examined whether (-) epigallocateocatechin-3- gallate (EGCG) or theaflavins (TF) could sensitize human cancer cells to CDDP via induction of apoptosis mediated by the inactivation of NF-κB and Akt signaling. Main methods Human cervical cancer cells (HeLa and SiHa cells) were treated with EGCG or TF and CDDP alone and with their combinations, further their effects on cell viability were evaluated. Western blotting was used for examining the apoptotic signaling proteins and inhibition of NF-κB activation. Levels of reactive oxygen species (ROS) production and mitochondria membrane potential (ΔΨm) were examined by flow cytometry. Key findings The combined treatment of EGCG or TF with CDDP elicited significant inhibition of cell growth in comparison to either of them in both cell lines (p < 0.05). Combinatorial treatment of both compounds potentially induced apoptosis by inhibiting the activation of Akt and NF-κB through blocking phosphorylation of inhibitor kappa Bα. These combinations acted in concert to induce increase in ROS level, release of cytochrome-c and expression of p53 and Bax, with decrease in cellular glutathione contents, ΔΨm, and Bcl-2 expression, thereby eventually resulting in the activation of caspases, poly(ADP)ribose polymerase cleavage and apoptosis of cancer cells. Significance Study suggests that both EGCG and TF chemosensitize the cervical cancer cells to CDDP-induced growth inhibition and apoptosis. By these combinations ~ 4 folds increase in CDDP induced-apoptosis with dose advantage of ~ 3 times could be achieved.
机译：目的组成性激活核因子-κB（NF-κB）和Akt参与化学耐药性以及抑制顺铂（CDDP）凋亡，因此，我们检查了（-）表没食子儿茶素-3-没食子酸酯（EGCG）或茶黄素（TF）可以通过诱导由NF-κB失活和Akt信号转导介导的凋亡诱导人类癌细胞对CDDP的敏感性。主要方法单独用EGCG或TF和CDDP及其组合治疗人宫颈癌细胞（HeLa和SiHa细胞），进一步评估其对细胞生存力的影响。 Western印迹用于检查细胞凋亡信号蛋白和对NF-κB激活的抑制。用流式细胞仪检测活性氧（ROS）的产生水平和线粒体膜电位（ΔΨm）。关键发现与两种细胞系中的任何一种相比，EGCD或TF与CDDP的联合治疗均引起细胞生长的显着抑制（p <0.05）。两种化合物的组合治疗可通过阻断抑制剂kappaBα的磷酸化来抑制Akt和NF-κB的活化，从而潜在地诱导细胞凋亡。这些组合协同作用诱导ROS水平增加，细胞色素c释放以及p53和Bax表达，同时细胞谷胱甘肽含量，ΔΨm和Bcl-2表达降低，从而最终导致胱天蛋白酶（poly（ ADP）核糖聚合酶切割和癌细胞凋亡。有意义的研究表明，EGCG和TF对宫颈癌细胞对CDDP诱导的生长抑制和凋亡具有化学敏感性。通过这些组合，可以使CDDP诱导的细胞凋亡增加约4倍，剂量优势达到约3倍。

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