Epicatechin attenuates doxorubicin-induced brain toxicity: Critical role of TNF-α, iNOS and NF-κB

被引：71

作者：

Mohamed, Rasha H. ^{[1
]}

Karam, Rehab A. ^{[2
]}

Amer, Mona G. ^{[3
]}

机构：

[1] Zagazig Univ, Fac Pharm, Dept Biochem, Zagazig 44511, Egypt

[2] Zagazig Univ, Fac Med, Dept Med Biochem, Zagazig 44511, Egypt

[3] Zagazig Univ, Fac Med, Dept Histol, Zagazig 44511, Egypt

来源：

BRAIN RESEARCH BULLETIN | 2011年 / 86卷 / 1-2期

关键词：

Doxorubicin; Epicatechin; Tumor necrosis factor alpha (TNF-alpha); Inducible NOS (iNOS); Nuclear factor kappa B (NF-kappa B); MANGANESE SUPEROXIDE-DISMUTASE; CENTRAL-NERVOUS-SYSTEM; NITRIC-OXIDE SYNTHASE; GREEN TEA CATECHINS; OXIDATIVE STRESS; LIPID-PEROXIDATION; ADRIAMYCIN; INDUCTION; INSIGHT; ACTIVATION;

D O I：

10.1016/j.brainresbull.2011.07.001

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Doxorubicin (DOX) is considered one of the most important chemotherapeutic agents that is used for the treatment of solid tumors. Its long-term use can cause neurodegenerative disorders due to its prolonged activation of microglia. The present study proved that the use of epicatechin prior to DOX treatment significantly attenuated not only the increase in TNF-alpha, iNOS and NF-kappa B expressions but also the increase in TNF-alpha and total nitrite levels in brain tissue when compared with rats treated with DOX-only. Thus, our study revealed that epicatechin can be used for the treatment of neuroinflammation and also for preventing the development of neurodegenerative disease during antineoplastic therapy because of its protective role in attenuation of neurotoxic pro-inflammatory mediators including TNF-alpha, NF-kappa B, and iNOS. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：22 / 28

页数：7

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