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抗坏血酸通过 MAPK 通路增强(-)-表没食子儿茶素-3-没食子酸酯和茶黄素-3,3'-双没食子酸酯诱导人肺腺癌细胞 SPC-A-1 和食管癌细胞 Eca-109 的细胞凋亡。

Enhancement of (-)-epigallocatechin-3-gallate and theaflavin-3-3'-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways.

机构信息

Department of Tea Science, Zhejiang University, 866 Yuhangtang Road, Hangzhou 310058, China.

出版信息

Biochem Biophys Res Commun. 2013 Aug 23;438(2):370-4. doi: 10.1016/j.bbrc.2013.07.078. Epub 2013 Jul 26.

Abstract

Tea polyphenols (-)-epigallocatechin-3-gallate (EGCG) and theaflavin-3-3'-digallate (TF3) are two prospective compounds in cancer prevention and treatment. Ascorbic acid (Vc) is essential to a healthy diet as well as being a highly effective antioxidant. In this work, the effects of the combination of EGCG or TF3 with Vc on the apoptosis and caspases-3/9 activities in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells were determined. Furthermore, the role of mitogen-activated protein kinases (MAPK) pathways in the apoptosis induced by TF3 or EGCG together with Vc were studied using three MAPK inhibitors (ERK inhibitor PD98059, JNK inhibitor SP600125 and p38 inhibitor SB203580). Our results showed that Vc could enhance the EGCG and TF3 induced apoptosis in SPC-A-1 and Eca-109 cells, and this effect involved the activation of caspase-3 and 9. EGCG, TF3 and Vc could activate MAPK pathways respectively, and each compound activated different MAPK subfamilies in different cells. This may explain the enhancement of EGCG and TF3 induced apoptosis by Vc in SPC-A-1 and Eca-109 cells, and will ultimately aid the design of more effective anti-cancer treatments.

摘要

茶多酚(-)-表没食子儿茶素-3-没食子酸酯(EGCG)和茶黄素-3,3'-双没食子酸酯(TF3)是癌症预防和治疗中两种有前景的化合物。抗坏血酸(Vc)是健康饮食所必需的,也是一种非常有效的抗氧化剂。在这项工作中,测定了 EGCG 或 TF3 与 Vc 联合对人肺腺癌细胞 SPC-A-1 和食管癌细胞 Eca-109 细胞凋亡和 caspase-3/9 活性的影响。此外,使用三种丝裂原活化蛋白激酶(MAPK)抑制剂(ERK 抑制剂 PD98059、JNK 抑制剂 SP600125 和 p38 抑制剂 SB203580)研究了 TF3 或 EGCG 与 Vc 共同诱导的 MAPK 通路在细胞凋亡中的作用。我们的结果表明,Vc 可以增强 EGCG 和 TF3 在 SPC-A-1 和 Eca-109 细胞中诱导的细胞凋亡,这种作用涉及 caspase-3 和 9 的激活。EGCG、TF3 和 Vc 可以分别激活 MAPK 通路,每种化合物在不同的细胞中激活不同的 MAPK 亚家族。这可以解释 Vc 在 SPC-A-1 和 Eca-109 细胞中增强 EGCG 和 TF3 诱导的细胞凋亡的作用,并最终有助于设计更有效的抗癌治疗方法。

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