التفاصيل البيبلوغرافية
| العنوان: |
Protective effects of dexpanthenol in carbon tetrachloride-induced myocardial toxicity in rats. |
| المؤلفون: |
Yildiz, Azibe, Demiralp, Tugba, Vardi, Nigar, Otlu, Gul, Taslidere, Elif, Cirik, Hilal, Gurel, Elif |
| المصدر: |
Tissue & Cell; Aug2022, Vol. 77, pN.PAG-N.PAG, 1p |
| مصطلحات موضوعية: |
CARBON tetrachloride, POLLUTANTS, TUMOR necrosis factors, TROPONIN I, VITAMIN B complex, LACTATE dehydrogenase |
| مستخلص: |
Exposure to various organic compounds including several environmental pollutants and drugs can cause cellular damage through the generation of lipid peroxidation products. Carbon tetrachloride (CCl 4) 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 CCl 4 -induced myocardial toxicity in rats. Administration of a single dose of CCl 4 caused cardiotoxicity by the increase in lipid peroxidation and histopathological changes (cardiomyocytes degeneration, interstitial edema) in the myocardial tissue. Moreover, CCl 4 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 CCl 4 treated group. Overall, this study suggests that Dxp is effective in inhibiting CCl 4 -induced lipid peroxidation, and that administration of Dxp may help prevent CCl 4 related inflammation, necrosis, and apoptosis on the cardiac tissue. • CCl 4 caused cardiotoxicity by the increase in lipid peroxidation in the myocardial tissue. • CCl 4 decreases LDH and troponin I immunoreactivity in cardiomyocytes. • CCl 4 increases TNF alpha and caspase-3 immunoreactivity. • Dxp treatment ameliorates CCl 4 -induced cardiomyocyte damage. • Dxp ameliorates myocardial damage with its anti-necrotic, anti-inflammatory and anti-apoptotic effects. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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