EGCG:肺癌治疗和化疗强化中的抗氧化剂

Amit Sehgal , Majaz Ahmad Bhat , Deeksha Dogra , Suman Rawat , Sunil Kumar Dhatwalia
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引用次数: 0

摘要

肺癌是全世界癌症相关死亡的主要原因。它的治疗包括密集的化疗和放疗周期,这与严重的不良反应有关。EGCG是绿茶/白茶中的一种活性成分,调节肿瘤干细胞凋亡、血管生成、增殖、分化和自我更新能力的细胞分子途径。它还可以作为一种促氧化剂,通过细胞凋亡导致癌细胞死亡。它可以通过改变Ras-GTPase、ERK、COX2、VEGF、蛋白激酶等多种信号转导通路中的分子来控制肺癌的发生。此外,它还可以影响其他信号分子或途径,如DNMT1、MAPK、NF-κB、Bcl/Bax、HIF-1α、EGFR、Akt/PI3、Wnt/β-catenin、caspases、NEAT1、TGF-β、HDGF、CLOCK。最近在细胞系和动物上的研究主要集中在EGCG在提高化疗药物疗效和减少其不良反应中的作用。EGCG的低生物利用度和快速代谢可能成为该药物从实验室到临床应用的障碍。合成药物如COMT抑制剂和纳米药物递送工具的使用已被证明可以提高血浆EGCG水平及其预防和治疗癌症的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EGCG: The antioxidant powerhouse in lung cancer management and chemotherapy enhancement

Lung cancer is the main cause of cancer-related deaths throughout the world. Its treatment involves intensive cycles of chemotherapy and radiotherapy, which are associated with serious adverse effects. EGCG, an active component of green tea/white tea, regulates cell molecular pathways of apoptosis, angiogenesis, proliferation, differentiation, and self-renewal ability of cancer stem cells. It also acts as a pro-oxidant that can cause cell death in cancer cells via apoptosis. It can control lung carcinogenesis by altering the molecules involved in multiple signal transduction pathways like Ras-GTPase, ERK, COX2, VEGF, and protein kinases. Moreover, it can also affect other signalling molecules or pathways such as DNMT1, MAPK, NF-κB, Bcl/Bax, HIF-1α, EGFR, Akt/PI3, Wnt/β-catenin, caspases, NEAT1, TGF-β, HDGF, and CLOCK. Recent studies on cell lines and animals have focused on the role of EGCG in enhancing the efficacy of chemotherapeutic drugs and reducing their adverse effects. The low bioavailability and rapid metabolism of EGCG can act as a hurdle in the translation of this agent from lab to bedside. The uses of synthetic agents such as COMT inhibitors and nano-drug delivery tools have been shown to enhance the plasma levels of EGCG and its cancer preventive and therapeutic ability.

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