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Differential Modulatory Effect of Epigallocatechin-3-Gallate in Suppression of Tumor Proliferation
Author(s) -
Ahmed Algazeery,
Ashraf S. A. El-Sayed,
Fatma Eldeeb,
Nomier Ma
Publication year - 2021
Publication title -
biomedical and pharmacology journal/biomedical and pharmacology journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.191
H-Index - 18
eISSN - 2456-2610
pISSN - 0974-6242
DOI - 10.13005/bpj/2216
Subject(s) - epigallocatechin gallate , pharmacology , antioxidant , green tea , polyphenol , cancer , chemistry , gallate , cancer research , dna damage , dna , biology , medicine , biochemistry , food science
Despite the remarkable progress in selecting the chemotherapeutic drugs, most are expensive and associated with many adverse effects targeting both cancer and normal cells. The using of polyphenols as natural materials for chemoprevention is considered a promising approach in reducing the tumor proliferation.This study aims to investigate whether a difference between the use of green tea and its component Epigallocatechin-gallate (EGCG) in treatment and protection against tumor. Sixty female Swiss albino mice weighted 20–22 g divided into 6 groups (n=10).The tumor suppression of green tea and EGCG was mirrored by evaluating their antioxidant and the anti-inflammatory effect on tumor markers and DNA integrity.Our results showed that the administration of EGCG showed a significant elevation of both antioxidants and anti-inflammatory markers in serum of EAC-bearing animals and revealed its high curative power to protect than treat tumor growth. Moreover, genomic DNA fragmentations assay present EGCG as a modulatory agent in keeping genome integrity.The administration of green tea and its major constituent EGCG showed a significant a potent protective role in suppressing tumor proliferation than its use in treatment due to its antioxidant and anti-inflammatory effect and maintaining the integrity of underlying genomic DNA that make it a strong barrier which arrest the process of oncogensis.

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