Sodium Ferulate Protects Against Daunorubicin-induced Cardiotoxicity by Inhibition of Mitochondrial Apoptosis in Juvenile Rats

Abstract

Daunorubicin (DNR) is a widely used chemotherapeutic agent; however, its clinical use is limited because of its cardiotoxicity. This study was aimed to investigate the protective effect of sodium ferulate (SF), an effective component from traditional Chinese herbs, against DNR-induced cardiotoxicity in juvenile rats. DNR was administered intraperitoneally to rats at the dosage of 2.5 mg·kg(-1)·wk(-1) for 5 consecutive weeks (cumulative dose of 12.5 mg/kg) or in combination with intraperitoneal injection of SF at 50 mg·kg(-1)·d(-1) over a period of 30 days. The animals were killed 6 days after the last injection of DNR. SF significantly ameliorated the DNR-induced cardiac dysfunction, structural damage of the myocardium, and release of lactate dehydrogenase and creatine kinase. Treatment with SF also reversed DNR-induced oxidative stress as evidenced by a decrease in malondialdehyde levels with a concomitant increase in myocardical superoxide dismutase activities. Furthermore, SF afforded significant cardioprotection against DNR-induced apoptosis in vivo and effectively suppressed the complex mitochondrion-dependent apoptotic signaling triggered by DNR. This study indicates that SF may improve cardiac function by inhibition of oxidative stress and apoptosis, thus providing a beneficial effect on the prevention of DNR-induced cardiotoxicity.

Protective effects of sodium ferulate on flap transplantation via anti-inflammatory modulation and oxidative stress inhibition

“…SF is a nonpeptide endothelin receptor antagonist, which can inhibit endothelin-induced vasoconstriction, blood pressure and vascular smooth muscle cell proliferation, reduce vascular endothelial damage, inhibit platelet aggregation, scavenge free radicals, and prevent lipid peroxidation. In the cardiovascular and cerebrovascular systems, digestive system, urinary system, central and peripheral nervous systems, visual system, and in ischemia-reperfusion injury in both animal experiments and clinical studies, SF shows large potential and versatile protective roles (18,19).…”

“…In normal tissues, endothelin and NO are in a state of balance. NO can counteract the vasoconstriction of endothelin, inhibit the formation of microthrombus, and avoid the occurrence of disseminated intravascular coagulation (8,(17)(18)(19). We found that the NO levels increased significantly in the SF group, and the mechanism of this phenomenon may be due to the specific endothelin receptor antagonist effect.…”

“…Neutrophils are activated, which adhere to vascular endothelial cells and cause the mechanical blockage of microvessels. They are also important sources of MPO, so an excess of neutrophils can increase MPO content in local tissues (8,(17)(18)(19).…”

Trans-Ferulic Acid-4-β-Glucoside Alleviates Cold-Induced Oxidative Stress and Promotes Cold Tolerance

“…The chemical structure is made up of ferulic acid and glucoside. Li Xia et al found that sodium ferulate improves energy metabolism and plays a protective role after myocardial ischemia reperfusion injury, while Wu et al suggested that ferulic acid protects the heart from lesion by inhibiting the apoptosis of mitochondria [25]. Pan Yiou et al found that ferulic acid inhibits lipid deposition in obese mice by mediating the expression of some important lipid metabolism genes.…”

Ferulic acid attenuates arsenic‐induced cardiotoxicity in rats

“…FA also possesses strong metal chelation activity [16], which could impart the cytoprotection. Moreover, FA exerts cardioprotection against isoproterenol [17], cyclophosphamide [18], streptozotocin [19], daunorubicin [20], and anoxia/reoxygenation [21] induced cardiotoxicity models. However, the effect of FA against As toxicity is very limited.…”