Key result
Molsidomine administered after doxorubicin reduced the incidence of ECG T negativity to 12.5% (1/8 rats) compared to 50% (4/8 rats) with doxorubicin alone, demonstrating cardioprotection.
Why the study?
Does molsidomine prevent or reduce doxorubicin-induced cardiotoxicity in rats?
RCT (n=40)
Randomized into five groups
Does molsidomine prevent or reduce doxorubicin-induced cardiotoxicity in rats?
Molsidomine demonstrates cardioprotective effects against doxorubicin-induced cardiotoxicity in a rat model by reducing oxidative stress and histological damage.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rats; leaves open any clinical role for molsidomine in doxorubicin cardiotoxicity.
PURPOSE: To explore the protective and curative effects of molsidomine (MOL) on doxorubicin (DOX)-induced cardiac damage in the in vivo rat heart. METHODS: Forty rats were randomized into five groups (n = 8): (1) the control group; (2) the MOL group (10 mg/kg for 21 days); (3) the DOX group (a single dose of 20 mg/kg); (4) the DOX + MOL group (3 days after the single dose of DOX, 10 mg/kg MOL continued for 21 days), and (5) the MOL + DOX group (24 h after a 21-day regimen of 10 mg/kg MOL, a single dose of DOX). The rats were monitored for mean arterial blood pressure, heart rate, O2 saturation, and electrocardiography. Heart tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and nitric oxide (NO) were determined. RESULTS: Blood pressure and O2 saturation values indicated a significant decrease in the DOX group compared with the control group. T negativity was observed in 4 of 8 rats in the DOX group, in 1 of 8 rats in the DOX + MOL group, and in 4 of 8 rats in the MOL + DOX group. MDA levels were significantly higher in the DOX group. SOD, GSH, and NO levels were significantly lower in the DOX group compared with the other groups. There was no statistically significant difference in the CAT levels in any of the study groups compared with controls. DOX treatment induced morphological alterations, such as disorganization of cardiomyocytes, loss of myofibrils, and cytoplasmic vacuolization in the heart. On the other hand, histological damage was significantly reduced in the DOX + MOL and MOL + DOX groups. CONCLUSION: This study implies that there are cardioprotective effects of MOL on DOX-induced cardiotoxicity.
No takes yet. Share an insight, caveat, or question.
Dişli et al. (2013) conducted an RCT in Doxorubicin-induced cardiotoxicity (n=40). Molsidomine vs. Doxorubicin alone and control was evaluated on ECG T negativity. Molsidomine administered after doxorubicin reduced the incidence of ECG T negativity to 12.5% (1/8 rats) compared to 50% (4/8 rats) with doxorubicin alone, demonstrating cardioprotection.
Synapse has enriched 10 related papers. Consider them for comparative context: