کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6262169 1613274 2011 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research reportEpicatechin attenuates doxorubicin-induced brain toxicity: Critical role of TNF-α, iNOS and NF-κB
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
Research reportEpicatechin attenuates doxorubicin-induced brain toxicity: Critical role of TNF-α, iNOS and NF-κB
چکیده انگلیسی

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-α, iNOS and NF-κB expressions but also the increase in TNF-α 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-α, NF-κB, and iNOS.

► The use of doxorubicin as chemotherapeutic agent can cause neurodegenerative disorders due to its prolonged activation of microglia. ► One of the major reasons for such disorders is the increase in TNF-α, iNOS and NF-κB expressions in brain tissue. ► This animal study proved that epicatechin can be used for the treatment of neuroinflammation through the decrease of such mediators.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research Bulletin - Volume 86, Issues 1–2, 10 August 2011, Pages 22-28
نویسندگان
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