The study focussed on the cardioprotective effect of
robinin on
doxorubicin-induced cardio-toxicity in Sprague Dawley rats. After the experimental period, animals were sacrificed and the various parameters such as cardiac markers, toxicity parameters,
antioxidant status, ROS generation, lipid peroxidation status and inflammatory parameters were assessed. Gene expression study by RT-PCR analysis and
proteins expression study by western blotting were done.
Doxorubicin causes significant increase in the levels of cardiac marker
enzymes, namely
lactate dehydrogenase (LDH),
creatine phospokinase (CPK), toxicity parameters like serum
glutamate oxaloacetate transaminase (
SGOT) and serum
glutamate pyruvate transaminase (
SGPT).
Antioxidant enzyme levels were decreased; lipid peroxidation products in heart tissue and inflammatory markers, namely
cyclooxygenase (COX2) and lipooxygenase (LOX15) were significantly increased. Gene expression study by RT-PCR analysis of transforming growth factor-β1 (TGF-β1), Smad2, murine double minute (Mdm2), Smad3,
cyclin-dependent kinase inhibitor 2A (CDKN2A), Smad4 and Smad7 were significantly altered. The western blotting study of p53, Bcl-2 and Bax also showed altered expression. The supplementation of the
Robinin along with DOX caused normalised level of all the above parameters and cardio-toxicity. This study revealed the cardioprotective nature of
Robinin on
doxorubicin-induced
cardiac toxicity by modulating TGF-β1 signaling pathway in Sprague Dawley rats.