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Abstract Title:

Protective effects of tannic acid on acute doxorubicin-induced cardiotoxicity: Involvement of suppression in oxidative stress, inflammation, and apoptosis.

Abstract Source:

Biomed Pharmacother. 2017 Sep ;93:1253-1260. Epub 2017 Jul 20. PMID: 28738542

Abstract Author(s):

Jianping Zhang, Lijing Cui, Xue Han, Yuanyuan Zhang, Xuan Zhang, Xi Chu, Fenghua Zhang, Ying Zhang, Li Chu

Article Affiliation:

Jianping Zhang

Abstract:

Doxorubicin (DOX) is a highly effective drug, but its cardiotoxicity restricts its therapeutic index. Oxidative stress is the major etiopathological factor in DOX-induced cardiotoxicity. Tannic acid (TA) has various anti-cancer, antioxidant, and anti-inflammatory activities. The purpose of the study was to survey the possible effects of TA against acute DOX-induced cardiotoxicity. Male Sprague-Dawleyrats were randomly divided into five groups: control, DOX (10mg/kg) alone, DOX with TA (20 and 40mg/kg), or DOX withcaptopril (30mg/kg) treatments. TA or captopril was administered once daily for six days, and DOX was injected intraperitoneally on the fourth day. TA significantlyattenuated DOX myocardial effects. Pretreatment with TA caused a decrease in levels of the serum enzymes lactate dehydrogenase, creatine kinase, and creatine kinase isoenzyme-MB to normal values. As indicators of oxidative stress, the levels of glutathione peroxidasesuperoxide dismutase and catalasesignificantly increased while the levels of malondialdehyde decreased after TA treatment. Additionally, DOX provoked inflammatory responses by causing anincrease in levels of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), endothelin (ET)-1 levels, and nuclear factor kappa-B (NF-κB) expression while TA pretreatment significantly inhibited TNF-α, IL-1β, ET-1, and NF-κB. Furthermore, DOX induced apoptosis by increasing bcl-2like protein and caspase-3 activities and c-fos andc-jun levels while causing a decrease in B-cell lymphoma-2 levels. Overall, there was evidence that TA could inhibit DOX-induced cardiotoxicity by inhibiting oxidative stress, inflammation and apoptotic damage.

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