Protective and therapeutic effects of dexpanthenol on isoproterenol-induced cardiac damage in rats.


Kalkan F., PARLAKPINAR H., DİŞLİ O. M., Tanriverdi L. H., ÖZHAN O., Polat A., ...Daha Fazla

Journal of cellular biochemistry, cilt.119, sa.9, ss.7479-7489, 2018 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 119 Sayı: 9
  • Basım Tarihi: 2018
  • Doi Numarası: 10.1002/jcb.27058
  • Dergi Adı: Journal of cellular biochemistry
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.7479-7489
  • Anahtar Kelimeler: cardiotoxicity, dexpanthenol, heart, isoproterenol, oxidative stress, INDUCED MYOCARDIAL INJURY, OXIDATIVE STRESS, PANTOTHENIC-ACID, AMINOGUANIDINE, GLUTATHIONE, ISCHEMIA, INFARCTION, MELATONIN, APOCYNIN, KIDNEY
  • İnönü Üniversitesi Adresli: Evet

Özet

The purpose of the study was to explore the protective and therapeutic effects of dexpanthenol (DEX) on isoproterenol (ISO)-induced cardiac damage. Forty rats were distributed into four groups: group I (Control); group II (ISO); ISO (150mg/kg/day) was given to rats once a day for 2 consecutive days with an interval of 24h; group III (DEX+ISO): DEX (250mg/kg) was applied 30min before the first ISO administration and continued in the next two days after second ISO administration; group IV (ISO+DEX): After the ISO treatment at 1st and 2nd days, DEX was given at 3rd and 4th days. Rats were monitored for mean arterial blood pressure (BP), heart rate, oxygen saturation (%SO2), and electrocardiography (ECG). Heart tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), reduced glutathione (GSH), total oxidant status (TOS); total antioxidant capacity (TAC), oxidative stress index (OSI), and caspase-3 were determined. BP and SO2 values indicated a significant decrease in the ISO group. Also, T wave negativity was observed in 6 of 10 rats, SOD, CAT, and GPX levels were significantly lower in ISO group than control group. ISO administration increased TOS and OSI levels, whereas DEX treatment significantly reduced these parameters. Also, ISO-induced morphological alterations such as disorganization of cardiomyocytes, loss of myofibrils and cytoplasmic vacuolization whereas these histological damages were significantly decreased in ISO+DEX and DEX+ISO groups when compared to the ISO group. This study implies the cardioprotective effects of DEX on ISO-induced cardiotoxicity.