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

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dc.authoridYildiz, Azibe/0000-0001-5686-7867
dc.authoridTaslidere, Elif/0000-0003-1723-2556
dc.authoridVardı, Nigar/0000-0003-0576-1696
dc.authorwosidYildiz, Azibe/ABI-7998-2020
dc.authorwosidTaslidere, Elif/ABI-8046-2020
dc.authorwosidVardı, Nigar/C-9549-2018
dc.contributor.authorYildiz, Azibe
dc.contributor.authorDemiralp, Tugba
dc.contributor.authorVardi, Nigar
dc.contributor.authorOtlu, Gul
dc.contributor.authorTaslidere, Elif
dc.contributor.authorCirik, Hilal
dc.contributor.authorGurel, Elif
dc.date.accessioned2024-08-04T20:51:59Z
dc.date.available2024-08-04T20:51:59Z
dc.date.issued2022
dc.departmentİnönü Üniversitesien_US
dc.description.abstractExposure 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.en_US
dc.identifier.doi10.1016/j.tice.2022.101824
dc.identifier.issn0040-8166
dc.identifier.pmid35653907en_US
dc.identifier.scopus2-s2.0-85131128444en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1016/j.tice.2022.101824
dc.identifier.urihttps://hdl.handle.net/11616/100682
dc.identifier.volume77en_US
dc.identifier.wosWOS:000807877200003en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherChurchill Livingstoneen_US
dc.relation.ispartofTissue & Cellen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCarbon tetrachlorideen_US
dc.subjectCardiotoxicityen_US
dc.subjectDexpanthenolen_US
dc.subjectHistopathologyen_US
dc.subjectImmunohistochemistryen_US
dc.subjectlipid peroxidationen_US
dc.titleProtective effects of dexpanthenol in carbon tetrachloride-induced myocardial toxicity in ratsen_US
dc.typeArticleen_US

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