Evaluation of protective effects of quercetin against cypermethrin-induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway

dc.authorid0000-0002-4581-4492
dc.authorid0000-0001-8884-4168
dc.authorid0000-0002-8490-2479
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKandemir, Özge
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2022-08-29T06:29:15Z
dc.date.available2022-08-29T06:29:15Z
dc.date.issued2022
dc.departmentTıp Fakültesi
dc.description.abstractCypermethrin (CYP), a type II synthetic pyrethroid, is the most widely used insecticide worldwide. Inhalation of it may cause side effects. This study is aimed to examine potential protection of quercetin (QUE) which is a well-known antioxidant in CYP-induced lung toxicity. Accordingly, 35 Spraque Dawley male rats were divided into five equal groups as follows: I-Control group, II-QUE group (50 mg/kg/b.w. QUE), III-CYP group (25 mg/kg/b.w. CYP), IV-CYP + QUE 25 (25 mg/kg/b.w. CYP + 25 mg/kg/b.w. QUE), V-CYP + QUE (25 mg/kg/b.w. CYP + 50 mg/kg/b.w. QUE) were treated with oral gavage throughout 28 days. CYP intoxication was associated with increased malondialdehyde level while glutathione concentration, activities of glutathione peroxidase, superoxide dismutase, and catalase reduced. CYP adminisitration caused of apoptosis in the lung by up-regulating caspase-3 and Bax levels and down-regulating Bcl-2. CYP also caused of endoplasmic reticulum (ER) stress by increasing mRNA transcript levels of PERK, IRE1, ATF6, and GRP78. Additionally, it was observed that CYP administration activated IL-6/JAK2/STAT3/MAPK14 signaling pathway and levels of IL-1?, NF-?B, TNF-?, and iNOS in the lung tissue. Therefore, it was determined that CYP administration triggered autophagy by upregulating LC3A and LC3B mRNA transcript levels. Moreover, the protein levels of NF-?B, caspase-3, Bax, Bcl-2, and cytochorme-c were examined by Western blot analysis. However, co-treatment with QUE at a dose of 25 and 50 mg/kg considerably protective oxidative stress, inflammation, apoptosis, ER stress, autophagy, and IL-6/JAK2/STAT3/MAPK14 signaling pathway in lung tissue. Overall, the findings of this study suggest that lung damage associated with CYP toxicity could be protected by QUE administration.
dc.identifier.doi10.1002/tox.23624
dc.identifier.endpage-en_US
dc.identifier.issn1520-4081
dc.identifier.issue-en_US
dc.identifier.pmid35876585
dc.identifier.scopusqualityQ1
dc.identifier.startpage-en_US
dc.identifier.urihttps:/dx.doi.org/10.1002/tox.23624
dc.identifier.urihttps://hdl.handle.net/20.500.12451/9647
dc.identifier.volume-en_US
dc.identifier.wosWOS:000829448800001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherJohn Wiley and Sons Inc
dc.relation.ispartofEnvironmental Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectCypermethrin
dc.subjectInflammation
dc.subjectLung Toxicity
dc.subjectOxidative Stress
dc.subjectQuercetin
dc.titleEvaluation of protective effects of quercetin against cypermethrin-induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway
dc.typeArticle

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