绿茶多酚通过时代性途径介导肠上皮细胞凋亡。

Helieh S Oz, Jeffrey L Ebersole
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引用次数: 0

摘要

结直肠癌是慢性炎症性肠病(IBD)患者最常见的恶性并发症。此外,由于目前使用的药物的细胞毒性作用,这些患者在化疗期间有发生痛苦并发症的风险。过去的研究表明,茶对胃肠道(GI)恶性肿瘤有保护作用。绿茶多酚(GrTP)抑制致癌物诱导的啮齿动物胃肠道肿瘤,并诱导多种癌细胞凋亡。我们假设GrTP及其多酚类化合物调节肠上皮细胞凋亡。在本研究中,研究了GrTP及其多酚类物质对肠上皮细胞(IEC-6)凋亡的影响。GrTP (400-800 mg/ml)诱导DNA断裂呈剂量依赖性。较高浓度(>800 mg/ml)诱导混合凋亡和细胞溶解。上皮细胞暴露于GrTP和主要多酚EGCG,而不是EGC或EC,以时间和剂量依赖的方式增加caspase活性。caspase抑制剂使细胞免于GrTP和egcg诱导的细胞死亡。同时,GrTP导致脂肪酸合成酶(Fas)-死亡结构域相关蛋白(FADD)的激活,并在治疗后30分钟募集到Fas/CD95结构域。虽然GrTP也阻断NF-κB的激活,但NF-κB抑制剂(MG132)仅促进细胞溶解。综上所述,这些数据表明GrTP和EGCG通过FADD依赖途径介导caspase-8诱导肠上皮细胞凋亡。未来的研究可能会保证GrTP在胃肠道恶性肿瘤中的预防和治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

GREEN TEA POLYPHENOLS MEDIATED APOPTOSIS IN INTESTINAL EPITHELIAL CELLS BY A FADD-DEPENDENT PATHWAY.

GREEN TEA POLYPHENOLS MEDIATED APOPTOSIS IN INTESTINAL EPITHELIAL CELLS BY A FADD-DEPENDENT PATHWAY.

GREEN TEA POLYPHENOLS MEDIATED APOPTOSIS IN INTESTINAL EPITHELIAL CELLS BY A FADD-DEPENDENT PATHWAY.

GREEN TEA POLYPHENOLS MEDIATED APOPTOSIS IN INTESTINAL EPITHELIAL CELLS BY A FADD-DEPENDENT PATHWAY.

Colorectal cancer is the most common malignant complication in patients with chronic inflammatory bowel disease (IBD). In addition, these patients are at risk for developing painful complications during chemotherapy due to cytotoxic effects of drugs currently in use. Past studies have suggested a protective effect of tea consumption on gastrointestinal (GI) malignancies. Green tea polyphenols (GrTP) inhibited carcinogen-induced GI tumors in rodents and induced apoptosis in various carcinoma cell lines. We hypothesized that GrTP and its polyphenolic compounds regulate apoptosis in the intestinal epithelia. In this study, the effects of GrTP and its polyphenolics on apoptosis was evaluated in intestinal epithelial, IEC-6, cells grown to 85% confluency. GrTP (400-800 mg/ml) induced DNA fragmentation in a dose dependent fashion. Higher concentrations (>800 mg/ml) induced a mixed apoptosis and cytolysis. Epithelial cells exposed to GrTP and a major polyphenol, EGCG, but not EGC or EC, increased caspase activities in a time and dose dependent manner. The caspase inhibitors rescued cells from GrTP and EGCG-induced cell death. Concomitantly, GrTP resulted in activation of fatty acid synthase (Fas)-associated protein with death domain (FADD) and recruitment to Fas/CD95 domain 30 minutes following treatment. While GrTP also blocked NF-κB activation, an NFκ-B inhibitor (MG132) only promoted cytolysis. In conclusion, these data demonstrated GrTP and EGCG induced apoptosis in intestinal epithelia mediated by caspase-8 through a FADD dependent pathway. Future investigation may warrant preventive as well as therapeutic strategies for GrTP in GI malignancy.

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