Antrodia cinnamomea Reduces Oxidative Injury and Protects Cardiac Histology in Doxorubicin-Induced Cardiotoxicity

Doxorubicin (DOX) cardiotoxicity is induced by oxidative stress and results in myocardial damage. We assessed the efficacy of Antrodia cinnamomea in alleviating DOX-induced cardiac injury in rats. Twenty-four male Sprague-Dawley rats were randomly assigned to one of four groups: Control, DOX (2 mg/kg i.p., every other day for 10 days), Antrodia cinnamomea (100 mg/kg p.o., daily), or DOX + Antrodia cinnamomea (2 mg/kg i.p., every other day for 10 days and 100 mg/kg p.o., daily). H&E was used to look at the hearts and give them a semi-quantitative injury score. We investigated malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) in left-ventricular homogenates. DOX caused a lot of damage to the heart muscle, disorganized myofibrils, created vacuoles in the cytoplasm, changed the shape of the nucleus, and caused interstitial edema. The injury scores were much higher than in the Control group (p <0.05). Biochemically, DOX elevated MDA levels while reducing SOD and GSH levels (p <0.05). Antrodia cinnamomea alone was similar to Control. Co-treatment (DOX + Antrodia cinnamomea) significantly reduced MDA and partially restored SOD and GSH in comparison to DOX (all p <0.05), which was consistent with lower histopathology scores; however, the values did not fully revert to Control levels. Antrodia cinnamomea lessens the cardiotoxicity caused by DOX by improving redox balance and protecting the structure of the heart muscle. These results support Antrodia cinnamomea as a potential adjunct to alleviate anthracycline cardiotoxicity and affirm the need for mechanistic and translational studies incorporating apoptosis/inflammation markers, ultrastructural validation, and pharmacokinetic profiling.