Key result
Treatment with pentoxifylline and cilostazol decreased troponin I, CK-MB, MDA, IL-6, TNF-α, and caspase-3 levels, and increased SOD activity, protecting against doxorubicin-induced cardiotoxicity.
Why the study?
Does pentoxifylline or cilostazol prevent doxorubicin-induced cardiotoxicity in a rat model?
Does pentoxifylline or cilostazol prevent doxorubicin-induced cardiotoxicity in a rat model?
Pentoxifylline and cilostazol demonstrate protective effects against doxorubicin-induced cardiotoxicity in a rat model by reducing cardiac injury biomarkers and inflammatory markers.
Hypothesis-generating in rats; leaves open translation to human doxorubicin cardiotoxicity prevention.
We investigated the possible protective effects of pentoxifylline (PTX) and cilostazol on doxorubicin (Dox)-induced cardiotoxicity in rats. Rats are randomly assigned into: saline, Dox (I.P. 2.5 mg/kg every other day six injections over two weeks), Dox (I.P. 2.5 mg/kg every other day six injections over two weeks then PTX (50 mg/kg/day/oral), Dox (I.P. 2.5 mg/kg) every other day six injections over two weeks then cilostazol (50 mg/kg/day/oral). After 21 days these animals were sacrificed and serum CK-MB and troponin I levels were determined. Malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and caspase-3 levels also were determined. Heart sections were examinedhistopathologically. Treatment with PTX and cilostazol decreased troponin I and CK-MB while increased SOD activity with decrements in MDA, IL-6, TNF-α, and caspase-3 levels with attenuation of the changes in cardiac histopathology. PTX and cilostazol exert protective effects against Dox-induced cardiotoxicity.
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Abbas et al. (2017) studied Doxorubicin-induced cardiotoxicity. Pentoxifylline and cilostazol vs. Saline and Doxorubicin alone was evaluated on Serum CK-MB, troponin I, MDA, SOD, TNF-α, IL-6, and caspase-3 levels, and cardiac histopathology. Treatment with pentoxifylline and cilostazol decreased troponin I, CK-MB, MDA, IL-6, TNF-α, and caspase-3 levels, and increased SOD activity, protecting against doxorubicin-induced cardiotoxicity.
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