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

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

TISSUE & CELL, vol.77, 2022 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 77
  • Publication Date: 2022
  • Doi Number: 10.1016/j.tice.2022.101824
  • Title of Journal : TISSUE & CELL
  • Keywords: Carbon tetrachloride, Cardiotoxicity, Dexpanthenol, Histopathology, Immunohistochemistry, lipid peroxidation, LIPID-PEROXIDATION, PANTOTHENIC-ACID, CHLOROGENIC ACID, LUNG INJURY, APOPTOSIS, GLUTATHIONE, MELATONIN, DAMAGE, LIVER


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.