Molecular docking analyses of Escin as regards cyclophosphamide-induced cardiotoxicity: In vivo and in Silico studies

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dc.authoridGUR, Fatma/0000-0001-5983-1472
dc.authoridCENGIZ, Mustafa/0000-0002-6925-8371
dc.contributor.authorGur, Fatma
dc.contributor.authorCengiz, Mustafa
dc.contributor.authorKutlu, Hatice Mehtap
dc.contributor.authorCengiz, Betul Peker
dc.contributor.authorAyhanci, Adnan
dc.date.accessioned2024-12-24T19:27:46Z
dc.date.available2024-12-24T19:27:46Z
dc.date.issued2021
dc.departmentSiirt Üniversitesi
dc.description.abstractThis study aims to investigate whether Escin (ES) can protect against Cyclophosphamide (CPM)-induced cardiac damage. The experimental rats were categorized as Control, CPM (200 mg/kg), ES (10 mg/kg), and CPM + ES Groups, each having 6 members. Their heart tissues were stained with Hematoxylin and Eosin and the structural changes were investigated under the light microscope. The biochemical markers of ischemia modified albumin (IMA), creatine kinase (CK-MB), antioxidant activity indicators Catalase (CAT), and superoxide dismutase (SOD) activities were measured using blood samples. Besides, the effects of CPM, ES, and CPM + ES upon CAT and SOD activities were shown via molecular docking studies. In the Single-Dose CPM group, CK-MB and IMA levels significantly increased while SOD and CAT levels significantly decreased. However, the heart tissues were damaged. CK-MB and IMA levels significantly decreased in CP+ ES Group. On the other hand, SOD, and CAT levels significantly increased and reduced the damage remarkably. Our findings showed that ES treatment successfully reduced the toxic effects upon the rats. The conclusion is that ES treatment can help protect the heart tissue against CPM-induced toxicity. Both in-vivo results and molecular modeling studies showed that the negative effects of CPM upon SOD activity were bigger than that of CAT.
dc.description.sponsorshipEskisehir Osmangazi University
dc.description.sponsorshipThe authors thank Eskisehir Osmangazi University for its generous support.
dc.identifier.doi10.1016/j.taap.2020.115386
dc.identifier.issn0041-008X
dc.identifier.issn1096-0333
dc.identifier.pmid33383042
dc.identifier.scopus2-s2.0-85098655132
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.taap.2020.115386
dc.identifier.urihttps://hdl.handle.net/20.500.12604/6788
dc.identifier.volume411
dc.identifier.wosWOS:000608793100001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ispartofToxicology and Applied Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241222
dc.subjectCyclophosphamide
dc.subjectEscin
dc.subjectCardiotoxicity
dc.subjectIschemia Modified Albumin
dc.subjectMolecular Modeling
dc.titleMolecular docking analyses of Escin as regards cyclophosphamide-induced cardiotoxicity: In vivo and in Silico studies
dc.typeArticle

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