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绿茶多酚通过依赖FADD的途径介导肠上皮细胞凋亡。

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

作者信息

Oz Helieh S, Ebersole Jeffrey L

机构信息

Center for Oral Health Research, College of Dentistry, University of Kentucky Medical Center, Lexington, KY.

出版信息

J Cancer Ther. 2010 Sep;1(3):105-113. doi: 10.4236/jct.2010.13018.

Abstract

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.

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具有细胞毒性作用,这些患者在化疗期间有发生疼痛性并发症的风险。过去的研究表明饮茶对胃肠道(GI)恶性肿瘤具有保护作用。绿茶多酚(GrTP)可抑制致癌物诱导的啮齿动物胃肠道肿瘤,并诱导各种癌细胞系凋亡。我们推测GrTP及其多酚类化合物可调节肠上皮细胞的凋亡。在本研究中,评估了GrTP及其多酚类化合物对生长至85%汇合度的肠上皮IEC-6细胞凋亡的影响。GrTP(400-800mg/ml)以剂量依赖性方式诱导DNA片段化。更高浓度(>800mg/ml)诱导混合性凋亡和细胞溶解。暴露于GrTP和主要多酚表没食子儿茶素没食子酸酯(EGCG)而非表儿茶素(EGC)或儿茶素(EC)的上皮细胞,以时间和剂量依赖性方式增加半胱天冬酶活性。半胱天冬酶抑制剂可使细胞免受GrTP和EGCG诱导的细胞死亡。同时,GrTP导致死亡结构域相关蛋白(FADD)与脂肪酸合酶(Fas)激活,并在处理后30分钟募集至Fas/CD95结构域。虽然GrTP也阻断核因子κB(NF-κB)激活,但NF-κB抑制剂(MG132)仅促进细胞溶解。总之,这些数据表明GrTP和EGCG通过FADD依赖性途径诱导半胱天冬酶-8介导的肠上皮细胞凋亡。未来的研究可能需要探索GrTP在胃肠道恶性肿瘤中的预防和治疗策略。

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