Archives of Physiology and Biochemistry · 2019 · 42 citations · 37 references
Life SciencesPharmacologyToxicologyBiochemical PharmacologyInflammationToxicodynamicsAnthracycline CardiotoxicityAntioxidant DefenseLipid PeroxidationMechanisms Of Toxic InjuryOxidative StressReactive Oxygen SpeciesCardiotoxicityDoxorubicin CardiotoxicityHyaline DegenerationMechanisms Of Cardiac InjuryOxidative Stress In Cardiovascular DiseaseOxidative Stress InjuryOxidative Stress ToxicityTissue Damage Mechanisms
The present study aims to examine the possible beneficial effects of gallic acid (GA) against doxorubicin-induced cardiotoxicity in the experimental model. Rats were weighed and divided into groups. Groups as following; control, gallic acid (GA), doxorubicin (DOX) and GA + DOX groups. At the end of the experiment, rats were sacrificed and heart tissue removed. The tissues were analysed in terms of biochemical (MDA, SOD, CAT, GSH, GPx), pathological (hyaline degeneration, Zenkerin necrosis, hyperaemia) and immunohistochemical (TNF-α, Cox-2). MDA level decreased and antioxidant enzyme activities increased in GA + DOX group compared to doxorubicin group. TNF-α, Cox-2 expression levels were severe in the DOX group. Also, pathologic tissue damage in heart tissue increased due to doxorubicin. Additionally, pathologic tissue damage and TNF-α, Cox-2 expression levels decreased in GA + DOX group. According to our findings, GA has protective effect against doxorubicin-induced cardiotoxicity.
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H. Aebi · Methods in enzymology on CD-ROM/Methods in enzymology · 1984 · 25.1K citations
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Jennifer Taylor · PubMed · 2012 · 587 citations