Sinapic acid protects against lead acetate-induced lung toxicity by reducing oxidative stress, apoptosis, inflammation, and endoplasmic reticulum stress damage

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dc.authorid0000-0002-8457-9448
dc.authorid0000-0002-8222-5515
dc.authorid0000-0001-6775-7858
dc.authorid0000-0002-4581-4492
dc.authorid0000-0002-8490-2479
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2024-07-02T08:38:21Z
dc.date.available2024-07-02T08:38:21Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractLead acetate (PbAc) is a compound that produces toxicity in many tissues after exposure. Sinapic acid (SNP) possesses many biological and pharmacological properties. This study aimed to investigate the efficacy of SNP on the toxicity of PbAc in lung tissue. PbAc was administered orally at 30 mg/kg and SNP at 5 or 10 mg/kg for 7 days. Biochemical, genetic, and histological methods were used to investigate inflammatory, apoptotic, endoplasmic reticulum stress, and oxidative stress damage levels in lung tissue. SNP administration induced PbAc-reduced antioxidant (GSH, SOD, CAT, and GPx) and expression of HO-1 in lung tissue. It also reduced MDA, induced by PbAc, and thus alleviated oxidative stress. SNP decreased the inflammatory markers NF-?B, TNF-? and IL-1? levels induced by PbAc in lung tissue and exhibited anti-inflammatory effect. PbAc increased apoptotic Bax, Apaf-1, and Caspase-3 mRNA transcription levels and decreased anti-apoptotic Bcl-2 in lung tissues. SNP decreased apoptotic damage by reversing this situation. On the other hand, SNP regulated these markers and brought them closer to the levels of the control group. PbAc caused prolonged ER stress by increasing the levels of ATF6, PERK, IRE1?, GRP78 and this activity was stopped and tended to retreat with SNP. After evaluating all the data, While PbAc caused toxic damage in lung tissue, SNP showed a protective effect by reducing this damage.
dc.identifier.doi10.1002/tox.24255
dc.identifier.endpage3832en_US
dc.identifier.issn1520-4081
dc.identifier.issue7en_US
dc.identifier.scopusqualityQ1
dc.identifier.startpage3820en_US
dc.identifier.urihttps:/dx.doi.org/10.1002/tox.24255
dc.identifier.urihttps://hdl.handle.net/20.500.12451/12015
dc.identifier.volume39en_US
dc.identifier.wosqualityN/A
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/openAccess
dc.subjectApoptosis
dc.subjectLead Acetate
dc.subjectLung Toxicity
dc.subjectOxidative Stress
dc.subjectsinapic Acid
dc.titleSinapic acid protects against lead acetate-induced lung toxicity by reducing oxidative stress, apoptosis, inflammation, and endoplasmic reticulum stress damage
dc.typeArticle

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