Comparative study of the protective effects of coenzyme Q10 and cinnamon extract on possible kidney damage and dysfunction of amiodarone in rats

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Background: An increase in free oxygen radicals and proinflammatory cytokines and decrease in intracellular adenosine triphosphate account for the nephrotoxic effect of amiodarone. This study investigated the protective effects of Coenzyme Q10 (CoQ10), cinnamon extract (CE) and the combination of the two (CoCE) on possible amiodarone-induced renal injury in rats. Methods: Thirty male albino Wistar rats were cetegorized into healthy (HG), amiodarone (ADG), CoQ10 + amiodarone (CoQA), CE + amiodarone (CEA), and CoCE + amiodarone (CoCEA) groups. First, CoQ10 (10 mg/kg) and CE (100 mg/kg) were orally given. After 1 h, 50 mg/kg amiodarone was orally given to all groups except for HG. Amiodarone, CoQ10, and CE administration was continued orally at the indicated doses once daily for 10 days.Then, blood samples were collected from all groups to determine creatinine, blood urea nitrogen (BUN), and kidney injury molecule (KIM-1) levels, followed by euthanasia and removal of kidney tissues. Oxidative stress and inflammatory parameters were analysed in the tissue samples. Histopathological examination was also performed on the tissues. Results: Amiodarone increased malondialdehyde levels and decreased total glutathione, superoxide dismutase, and catalase levels (p < 0.001). Amiodarone increased the expression and tissue levels of tissue nuclear factor kappa B, tumor necrosis factor-alpha, interleukin-1β and interleukin-6, and led to increases in serum creatinine and BUN and KIM-1 levels (p < 0.001). Amiodarone also caused histopathological damage (p < 0.001).CoQ10, CE and especially CoCE inhibited biochemical changes and tissue damage (p < 0.001). Conclusion: Although CoQ10, CE, and CoCE effectively prevent amiodarone-induced oxidative and inflammatory nephrotoxicity, CoCE appears to be superior. © The Author(s), under exclusive licence to Japanese Society of Nephrology 2024.

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https://rdlopen.rawdatalibrary.net/r/ebyu/10859Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1007/s10157-024-02584-6Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorEkici, Ozgur
dc.contributor.authorGul, Abdullah
dc.contributor.authorKeskin, Ercument
dc.contributor.authorBulut, Seval
dc.contributor.authorSuleyman, Bahadir
dc.contributor.authorMammadov, Renad
dc.contributor.authorCicek, Betul
dc.contributor.authorDemir, Ozlem
dc.contributor.authorGunay, Murat
dc.contributor.authorSuleyman, Halis
dc.date.accessioned2026-10-18T20:25:58.965959726Z
dc.date.available2026-10-18T20:25:58.965959726Z
dc.date.issued2025
dc.description.abstractBackground: An increase in free oxygen radicals and proinflammatory cytokines and decrease in intracellular adenosine triphosphate account for the nephrotoxic effect of amiodarone. This study investigated the protective effects of Coenzyme Q10 (CoQ10), cinnamon extract (CE) and the combination of the two (CoCE) on possible amiodarone-induced renal injury in rats. Methods: Thirty male albino Wistar rats were cetegorized into healthy (HG), amiodarone (ADG), CoQ10 + amiodarone (CoQA), CE + amiodarone (CEA), and CoCE + amiodarone (CoCEA) groups. First, CoQ10 (10 mg/kg) and CE (100 mg/kg) were orally given. After 1 h, 50 mg/kg amiodarone was orally given to all groups except for HG. Amiodarone, CoQ10, and CE administration was continued orally at the indicated doses once daily for 10 days.Then, blood samples were collected from all groups to determine creatinine, blood urea nitrogen (BUN), and kidney injury molecule (KIM-1) levels, followed by euthanasia and removal of kidney tissues. Oxidative stress and inflammatory parameters were analysed in the tissue samples. Histopathological examination was also performed on the tissues. Results: Amiodarone increased malondialdehyde levels and decreased total glutathione, superoxide dismutase, and catalase levels (p < 0.001). Amiodarone increased the expression and tissue levels of tissue nuclear factor kappa B, tumor necrosis factor-alpha, interleukin-1β and interleukin-6, and led to increases in serum creatinine and BUN and KIM-1 levels (p < 0.001). Amiodarone also caused histopathological damage (p < 0.001).CoQ10, CE and especially CoCE inhibited biochemical changes and tissue damage (p < 0.001). Conclusion: Although CoQ10, CE, and CoCE effectively prevent amiodarone-induced oxidative and inflammatory nephrotoxicity, CoCE appears to be superior. © The Author(s), under exclusive licence to Japanese Society of Nephrology 2024.
dc.identifier.doi10.1007/s10157-024-02584-6
dc.identifier.eissn1437-7799
dc.identifier.endpage426
dc.identifier.issn1342-1751
dc.identifier.issue4
dc.identifier.pmid39476229
dc.identifier.scopus2-s2.0-85207919160
dc.identifier.startpage414
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/10859
dc.identifier.volume29
dc.identifier.wosWOS:001346008600001
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofClinical and Experimental Nephrology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAnti-inflammatory
dc.subjectAntiarrhythmic
dc.subjectAntioxidant
dc.subjectNephrotoxicity
dc.subjectProinflammatory cytokine
dc.subjectAmiodarone
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectBlood Urea Nitrogen
dc.subjectCell Adhesion Molecules
dc.subjectCinnamomum zeylanicum
dc.subjectCreatinine
dc.subjectGlutathione
dc.subjectKidney
dc.subjectKidney Diseases
dc.subjectMale
dc.subjectMalondialdehyde
dc.subjectOxidative Stress
dc.subjectPlant Extracts
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectUbiquinone
dc.subjectadenosine triphosphate
dc.subjectantiarrhythmic agent
dc.subjectcatalase
dc.subjectcinnamon extract
dc.subjectcytokine
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.titleComparative study of the protective effects of coenzyme Q10 and cinnamon extract on possible kidney damage and dysfunction of amiodarone in rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus1
rdl.citation.wos1
rdl.departmentDepartment of Urology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey. | Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey. | Department of Physiology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey. | Department of Histology and Embryology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey. | Biochemistry Laboratory, Erzincan Mengücek Gazi Training and Research Hospital, Erzincan Binali Yildirim University, Erzincan, Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)