The protective effects of chrysin on cadmium-induced pulmonary toxicity; a multi-biomarker approach

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dc.authorid0000-0002-8457-9448
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorGür, Cihan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorÖz, Mehmet
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2023-09-29T06:14:27Z
dc.date.available2023-09-29T06:14:27Z
dc.date.issued2023
dc.departmentTıp Fakültesi
dc.description.abstractThis study aimed to determine the potential protective effects of chrysin (CHR) on experimental cadmium (Cd)-induced lung toxicity in rats. To this end, rats were divided into five groups; Control, CHR, Cd, Cd + CHR25, Cd + CHR50. In the study, rats were treated with CHR (oral gavage, 25 mg/kg and 50 mg/kg) 30 min after giving Cd (oral gavage, 25 mg/kg) for 7 consecutive days. The effects of Cd and CHR treatments on oxidative stress, inflammatory response, ER stress, apoptosis and tissue damage in rat lung tissues were determined by biochemical and histological methods. Our results revealed that CHR therapy for Cd-administered rats could significantly reduce MDA levels in lung tissue while significantly increasing the activity of antioxidant enzymes (SOD, CAT, GPx) and GSH levels. CHR agent exerted antiinflammatory effect by lowering elevated levels of NF-?B, IL-1? IL-6, TNF-?, RAGE and NRLP3 in Cd-induced lung tissue. Moreover CHR down-regulated Cd-induced ER stress markers (PERK, IRE1, ATF6, CHOP, and GRP78) and apoptosis markers (Caspase-3, Bax) lung tissue. CHR up-regulated the Bcl-2 gene, an anti-apoptotic marker. Besides, CHR attenuated the side effects caused by Cd by modulating histopathological changes such as hemorrhage, inflammatory cell infiltration, thickening of the alveolar wall and collagen increase. Immunohistochemically, NF-?B and Caspase-3 expressions were intense in the Cd group, while these expressions were decreased in the Cd + CHR groups. These results suggest that CHR exhibits protective effects against Cd-induced lung toxicity in rats by ameliorating oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and histological changes.
dc.identifier.doi10.1007/s11356-023-28747-8
dc.identifier.endpage89494en_US
dc.identifier.issn0944-1344
dc.identifier.issue38en_US
dc.identifier.scopusqualityQ1
dc.identifier.startpage89479en_US
dc.identifier.urihttps:/dx.doi.org10.1007/s11356-023-28747-8
dc.identifier.urihttps://hdl.handle.net/20.500.12451/11006
dc.identifier.volume30en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer Science and Business Media Deutschland GmbH
dc.relation.ispartofEnvironmental Science and Pollution Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectApoptosis
dc.subjectCadmium
dc.subjectChrysin
dc.subjectEndoplasmic Reticulum Stress
dc.subjectInflammation
dc.subjectLung Injury
dc.titleThe protective effects of chrysin on cadmium-induced pulmonary toxicity; a multi-biomarker approach
dc.typeArticle

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