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

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-α) 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.