Trigonelline alkaloid is effective in preventing doxorubicin-induced lung damage

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Background: One of the most popular chemotherapy medications is doxorubicin (DOX), however it can have non-negligible damage. When the underlying mechanisms of damage are investigated, the most prominent pathways are oxidative stress, inflammation and apoptosis. Aim: We investigated the NF-κB/MAPK inflammatory pathway and cellular apoptosis to determine the efficacy of trigonelline alkaloid (TRIG) in preventing DOX-induced lung injury. Methodology: The study consisted of C, TRIG, DOX and TRIG+DOX groups. TRIG and TRIG+DOX groups received 50 mg/kg TRIG for 7 days. On day 8, DOX and TRIG+DOX groups received a single dose of 15 mg/kg DOX. Results: Our results showed that apoptosis markers and inflammation were higher in the DOX group. In contrast, TRIG pretreatment partially suppressed apoptosis and decreased inflammation by blocking the activation of the MAPK/NF-κB pathway, lowering IL-6 levels, and protecting the lung from apoptotic cell death. Conclusion: Assessing TRIG’s effectiveness in lung tissue injury, this study may be a crucial first step. © 2024 Informa UK Limited, trading as Taylor & Francis Group.

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AlanDeğerDil
dc.contributor.authorUslu, Hamit
dc.contributor.authorAtila Uslu, Gözde
dc.contributor.authorÇiçek, Betül
dc.contributor.authorBolat, İsmail
dc.contributor.authorYıldırım, Serkan
dc.date.accessioned2026-10-18T20:26:31.445217327Z
dc.date.available2026-10-18T20:26:31.445217327Z
dc.date.issued2025
dc.description.abstractBackground: One of the most popular chemotherapy medications is doxorubicin (DOX), however it can have non-negligible damage. When the underlying mechanisms of damage are investigated, the most prominent pathways are oxidative stress, inflammation and apoptosis. Aim: We investigated the NF-κB/MAPK inflammatory pathway and cellular apoptosis to determine the efficacy of trigonelline alkaloid (TRIG) in preventing DOX-induced lung injury. Methodology: The study consisted of C, TRIG, DOX and TRIG+DOX groups. TRIG and TRIG+DOX groups received 50 mg/kg TRIG for 7 days. On day 8, DOX and TRIG+DOX groups received a single dose of 15 mg/kg DOX. Results: Our results showed that apoptosis markers and inflammation were higher in the DOX group. In contrast, TRIG pretreatment partially suppressed apoptosis and decreased inflammation by blocking the activation of the MAPK/NF-κB pathway, lowering IL-6 levels, and protecting the lung from apoptotic cell death. Conclusion: Assessing TRIG’s effectiveness in lung tissue injury, this study may be a crucial first step. © 2024 Informa UK Limited, trading as Taylor & Francis Group.
dc.identifier.doi10.1080/13813455.2024.2404097
dc.identifier.eissn1744-4160
dc.identifier.endpage176
dc.identifier.issn1381-3455
dc.identifier.issue2
dc.identifier.pmid39287053
dc.identifier.scopus2-s2.0-105001345757
dc.identifier.startpage169
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/11476
dc.identifier.volume131
dc.identifier.wosWOS:001314376900001
dc.language.isoen
dc.publisherTaylor and Francis Ltd.
dc.relation.ispartofArchives of Physiology and Biochemistry
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectapoptosis
dc.subjectDoxorubicin
dc.subjectinflammation
dc.subjectNF-κB/MAPK
dc.subjecttrigonelline alkaloid
dc.subjectAlkaloids
dc.subjectAnimals
dc.subjectInterleukin-6
dc.subjectLung
dc.subjectLung Injury
dc.subjectMale
dc.subjectMAP Kinase Signaling System
dc.subjectNF-kappa B
dc.subjectOxidative Stress
dc.subjectalkaloid
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinterleukin 6
dc.subjecttrigonelline
dc.subjectanimal
dc.subjectdrug effect
dc.subjectMAPK signaling
dc.subjectmetabolism
dc.subjectpathology
dc.subjectprevention and control
dc.titleTrigonelline alkaloid is effective in preventing doxorubicin-induced lung damage
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus6
rdl.citation.wos6
rdl.departmentDepartment of Physiology, Erzincan Binali Yıldırım University, Erzincan, Türkiye.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)