title: Effects of molsidomine against doxorubicin-induced cardiotoxicity in rats.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  This study implies that there are cardioprotective effects of MOL on DOX-induced cardiotoxicity.
authors.affiliation: Department of Cardiovascular Surgery, Inonu University Faculty of Medicine, Malatya, Turkey.
authors.forename: O M
authors.initials: OM
authors.lastname: Disli
authors.forename: E
authors.initials: E
authors.lastname: Sarihan
authors.forename: M C
authors.initials: MC
authors.lastname: Colak
authors.forename: N
authors.initials: N
authors.lastname: Vardi
authors.forename: A
authors.initials: A
authors.lastname: Polat
authors.forename: J
authors.initials: J
authors.lastname: Yagmur
authors.forename: B
authors.initials: B
authors.lastname: Tamtekin
authors.forename: H
authors.initials: H
authors.lastname: Parlakpinar
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D002374:Catalase / Q000378:metabolism; D004317:Doxorubicin / Q000633:toxicity*; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D008981:Molsidomine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D000903:Antibiotics, Antineoplastic; D014665:Vasodilator Agents; D004317:Doxorubicin; D008981:Molsidomine; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione