Chemopreventive and Chemosensitizing Effects of Green Tea: An Evidence-based Review

被引：1

作者：

Gul, Sameena ^{[1
]}

Hassan, Sayyeda Hira ^{[1
]}

Maryam, Amara ^{[1
]}

Shakir, Hafiz Abdullah ^{[1
]}

Khan, Muhammad ^{[1
]}

Irfan, Muhammad ^{[2
]}

Shakoori, Farah Rauf ^{[1
]}

Qazi, Javed Iqbal ^{[1
]}

机构：

[1] Univ Punjab, Dept Zool, Quaid E Azam Campus, Lahore 54590, Pakistan

[2] Univ Sargodha, Dept Biotechnol, Sargodha, Pakistan

来源：

PAKISTAN JOURNAL OF ZOOLOGY | 2022年 / 54卷 / 05期

关键词：

EGCG; Camellia sinensis; Anticancer; Chemo-sensitization; Apoptosis; CANCER DRUG-RESISTANCE; PROSTATE-CANCER; EPIGALLOCATECHIN GALLATE; MULTIDRUG-RESISTANCE; P-GLYCOPROTEIN; LIVER-CANCER; LUNG-CANCER; BLACK TEA; CELLS; APOPTOSIS;

D O I：

10.17582/journal.pjz/20191021131001

中图分类号：

Q95 [动物学];

学科分类号：

071002 ;

摘要：

Cancer is a major health problem and second foremost cause of death globally. Chemotherapy either targeted or non-targeted is pervasive in the treatment of cancer but due to continuous and repeated doses, cancer cells develop resistance against these chemotherapeutic drugs through multiple mechanisms including MDR1 gene expression. EGCG (Epigallocatechin-3-Gallate) is one of the major polyphenols present in the dry leaves of green tea plant (Camellia sinensis). It has been observed to potentiate the apoptosis and also inhibit cancer cell growth by affecting various signaling molecules and cell cycle regulatory proteins. Clinical studies demonstrated that EGCG treatment of different type of cancers has synergistic effect in combination treatment with other common clinical drugs (cisplatin, taxol, doxorubicin and vinblastine) by modulating chemotherapy response to cancer cells as compared to clinical drugs alone. This review enlightens the possible mechanisms by which EGCG overcome chemo-resistance and recover efficacy of many clinical drugs in various human cancers.

引用

页码：2425 / 2436

页数：12

共 81 条

[11] Epigallocatechin gallate and sulforaphane combination treatment induce apoptosis in paclitaxel-resistant ovarian cancer cells through hTERT and Bcl-2 down-regulation [J].