Protective effects of dexpanthenol in carbon tetrachloride-induced myocardial toxicity in rats


YILDIZ A., Demiralp T., VARDI N., Otlu G., TAŞLIDERE E., Cirik H., ...Daha Fazla

TISSUE & CELL, cilt.77, 2022 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 77
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1016/j.tice.2022.101824
  • Dergi Adı: TISSUE & CELL
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: Carbon tetrachloride, Cardiotoxicity, Dexpanthenol, Histopathology, Immunohistochemistry, lipid peroxidation, LIPID-PEROXIDATION, PANTOTHENIC-ACID, CHLOROGENIC ACID, LUNG INJURY, APOPTOSIS, GLUTATHIONE, MELATONIN, DAMAGE, LIVER
  • İnönü Üniversitesi Adresli: Evet

Özet

Exposure to various organic compounds including several environmental pollutants and drugs can cause cellular damage through the generation of lipid peroxidation products. Carbon tetrachloride (CCl4) is a potent toxic agent that causes peroxidative degeneration in many tissues. Dexpanthenol (Dxp) is a member of the B complex vitamins that exhibits antioxidant effects against lipid peroxidation products. This study was designed to evaluate the cardioprotective effect of Dxp against CCl4-induced myocardial toxicity in rats. Administration of a single dose of CCl4 caused cardiotoxicity by the increase in lipid peroxidation and histopathological changes (cardiomyocytes degeneration, interstitial edema) in the myocardial tissue. Moreover, CCl4 caused a decrease in lactate dehydrogenase (LDH) and troponin-I immunoreactivities, while significantly increasing tumor necrosis factor-alpha (TNF-alpha) and caspase-3 immunoreactivities. On the other hand, administration of Dxp improved biochemical, histopathological, and immunohistochemical parameters compared to the CCl4 treated group. Overall, this study suggests that Dxp is effective in inhibiting CCl4-induced lipid peroxidation, and that administration of Dxp may help prevent CCl4 related inflammation, necrosis, and apoptosis on the cardiac tissue.