Protective effect of cinnamon extract against cobalt-induced multiple organ damage in rats

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Background: The role of oxidative stress and inflammation in cobalt (Co) toxicity has been the focus of previous studies. Cinnamon and its main components have been reported to have protective effects in various tissues with antioxidant and anti-inflammatory effects. Aims: In this study, the protective effect of cinnamon extract (CE) against possible Co-induced heart, kidney, and liver damage in rats was investigated biochemically. Methods: Eighteen albino Wistar-type male rats were categorized into three groups (n = 6 per group): control (CG), CoCL2-administered (CoCL2), and CE + CoCL2-administered (CE + Co) groups. The CE + CoCL2 group was administered CE (100 mg/kg), and the CoCL2 and CG groups were administered distilled water orally by gavage. One hour after the administration, Co (150 mg/kg) was administered orally to the CE + CoCL2 and CoCL2 groups. This procedure was repeated once daily for 7 days. Then, biochemical markers were studied in the excised heart, kidney, and liver tissues. Results: CoCL2 increased oxidants and proinflammatory cytokines and decreased antioxidants in heart, kidney, and liver tissues. Heart, kidney, and liver tissue were affected by Co damage. CE treatment suppressed the CoCL2-induced increase in oxidants and proinflammatory cytokines and decrease in antioxidants in heart, kidney, and liver tissues. CE treatment has been shown to attenuate cardiac damage by reducing serum troponin I (TpI) and creatine kinase-MB (CK-MB), renal damage by reducing creatinine and blood urea nitrogen (BUN), and liver damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Conclusion: Co induced the production of oxidants and proinflammatory parameters and antioxidant depletion in heart, kidney, and liver tissues of rats. Our experimental results show that CE protects heart, kidney, and liver tissues against oxidative and inflammatory changes induced by CoCLl2. Copyright © 2024 Isik, Suleyman, Mammadov, Bulut, Yavuzer, Altuner, Coban and Suleyman.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/11744Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.3389/fphar.2024.1384181Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorIsik, Bahar
dc.contributor.authorSuleyman, Bahadir
dc.contributor.authorMammadov, Renad
dc.contributor.authorBulut, Seval
dc.contributor.authorYavuzer, Bulent
dc.contributor.authorAltuner, Durdu
dc.contributor.authorCoban, Taha Abdulkadir
dc.contributor.authorSuleyman, Halis
dc.date.accessioned2026-10-18T20:26:44.670495514Z
dc.date.available2026-10-18T20:26:44.670495514Z
dc.date.issued2024
dc.description.abstractBackground: The role of oxidative stress and inflammation in cobalt (Co) toxicity has been the focus of previous studies. Cinnamon and its main components have been reported to have protective effects in various tissues with antioxidant and anti-inflammatory effects. Aims: In this study, the protective effect of cinnamon extract (CE) against possible Co-induced heart, kidney, and liver damage in rats was investigated biochemically. Methods: Eighteen albino Wistar-type male rats were categorized into three groups (n = 6 per group): control (CG), CoCL2-administered (CoCL2), and CE + CoCL2-administered (CE + Co) groups. The CE + CoCL2 group was administered CE (100 mg/kg), and the CoCL2 and CG groups were administered distilled water orally by gavage. One hour after the administration, Co (150 mg/kg) was administered orally to the CE + CoCL2 and CoCL2 groups. This procedure was repeated once daily for 7 days. Then, biochemical markers were studied in the excised heart, kidney, and liver tissues. Results: CoCL2 increased oxidants and proinflammatory cytokines and decreased antioxidants in heart, kidney, and liver tissues. Heart, kidney, and liver tissue were affected by Co damage. CE treatment suppressed the CoCL2-induced increase in oxidants and proinflammatory cytokines and decrease in antioxidants in heart, kidney, and liver tissues. CE treatment has been shown to attenuate cardiac damage by reducing serum troponin I (TpI) and creatine kinase-MB (CK-MB), renal damage by reducing creatinine and blood urea nitrogen (BUN), and liver damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Conclusion: Co induced the production of oxidants and proinflammatory parameters and antioxidant depletion in heart, kidney, and liver tissues of rats. Our experimental results show that CE protects heart, kidney, and liver tissues against oxidative and inflammatory changes induced by CoCLl2. Copyright © 2024 Isik, Suleyman, Mammadov, Bulut, Yavuzer, Altuner, Coban and Suleyman.
dc.identifier.doi10.3389/fphar.2024.1384181
dc.identifier.eissn1663-9812
dc.identifier.issn1663-9812
dc.identifier.pmcidPMC11111945
dc.identifier.pmid38783942
dc.identifier.scopus2-s2.0-85193807896
dc.identifier.startpage1384181
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/11744
dc.identifier.volume15
dc.identifier.wosWOS:001228999100001
dc.language.isoen
dc.publisherFrontiers Media SA
dc.relation.ispartofFrontiers in Pharmacology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectcinnamon
dc.subjectcobalt
dc.subjectheart
dc.subjectkidney
dc.subjectliver
dc.subjectoxidative damage
dc.subjectalanine aminotransferase
dc.subjectantioxidant
dc.subjectaspartate aminotransferase
dc.subjectbiological marker
dc.subjectcatalase
dc.subjectcinnamon extract
dc.subjectcreatine kinase MB
dc.subjectcreatinine
dc.subjectcytokine
dc.subjectglutathione peroxidase
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectketamine
dc.subjectmalonaldehyde
dc.subjectoxidizing agent
dc.subjectsuperoxide dismutase
dc.subjecttroponin I
dc.subjecttumor necrosis factor
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbiochemical analysis
dc.subjectblood sampling
dc.titleProtective effect of cinnamon extract against cobalt-induced multiple organ damage in rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus4
rdl.citation.wos3
rdl.departmentDepartment of Emergency Medicine, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye. | Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye. | Department of Medical Biochemistry, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)