Possible Neuroprotective Effect of tDCS on Doxorubicin-Induced Neurotoxicity in Rats

ArticleAçık Erişim

Özet

Doxorubicin (DOX), a chemotherapeutic medicine, are frequently utilized to treat various malignancies, even though it has well-documented negative side effects. Neurotoxic effect is one of the best known and occurs through several mechanisms including oxidative stress and neuro-inflammation. Transcranial direct current stimulation (tDCS), a non-invasive brain stimulation technique, is used in several neurodegenerative disease model because of its neuroprotective effects. The aim of this study was to investigate the effects of DOX on antioxidant and inflammatory markers, behavioral parameters and the possible neuroprotective effect of tDCS stimulation on these effects. To induce neurotoxicity, DOX was administered intraperitoneally (i.p.) at 2.15 mg/kg/day, 1 dose in 3 days, 7 times in total for 3 weeks. tDCS treatment was then applied for 5 consecutive days. Catalase (CAT), interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and interleukin 6 (IL-6) levels were evaluated. Open field test was used to analyzed to locomotor activity and behavioral changes. The DOX group had neuronal alteration as indicated by the elevation of neuro-inflammation markers (IL-1 beta, TNF-alpha, and IL-6) with reduced antioxidant marker (CAT). The tDCS-treated group showed a significant reduction in the inflammation biomarkers, with a significant improvement in the antioxidant marker. DOX administration impaired locomotor activity as well as anxiety behaviors of rats. tDCS have also been shown to be effective in preventing behavioral and locomotor changes; therefore, they may be considered as candidates to reduce toxicity effects in DOX treatments. Our findings reveal the importance of tDCS treatment to attenuate DOX-associated neurotoxicity. Through the modification and decrease of indicators of cellular toxicity and the increase of natural antioxidant enzymes, tDCS demonstrated considerable promise for avoiding DOX-induced neurotoxicity.

Anahtar Kelimeler

RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/17062Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1134/s1819712425700205Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorDanisman, Betul
dc.contributor.authorGokce, Yasin
dc.contributor.authorCicek, Betul
dc.contributor.authorGul, Deniz Kantar
dc.contributor.authorDerin, Narin
dc.date.accessioned2026-10-18T20:42:59.705334065Z
dc.date.available2026-10-18T20:42:59.705334065Z
dc.date.issued2025
dc.description.abstractDoxorubicin (DOX), a chemotherapeutic medicine, are frequently utilized to treat various malignancies, even though it has well-documented negative side effects. Neurotoxic effect is one of the best known and occurs through several mechanisms including oxidative stress and neuro-inflammation. Transcranial direct current stimulation (tDCS), a non-invasive brain stimulation technique, is used in several neurodegenerative disease model because of its neuroprotective effects. The aim of this study was to investigate the effects of DOX on antioxidant and inflammatory markers, behavioral parameters and the possible neuroprotective effect of tDCS stimulation on these effects. To induce neurotoxicity, DOX was administered intraperitoneally (i.p.) at 2.15 mg/kg/day, 1 dose in 3 days, 7 times in total for 3 weeks. tDCS treatment was then applied for 5 consecutive days. Catalase (CAT), interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and interleukin 6 (IL-6) levels were evaluated. Open field test was used to analyzed to locomotor activity and behavioral changes. The DOX group had neuronal alteration as indicated by the elevation of neuro-inflammation markers (IL-1 beta, TNF-alpha, and IL-6) with reduced antioxidant marker (CAT). The tDCS-treated group showed a significant reduction in the inflammation biomarkers, with a significant improvement in the antioxidant marker. DOX administration impaired locomotor activity as well as anxiety behaviors of rats. tDCS have also been shown to be effective in preventing behavioral and locomotor changes; therefore, they may be considered as candidates to reduce toxicity effects in DOX treatments. Our findings reveal the importance of tDCS treatment to attenuate DOX-associated neurotoxicity. Through the modification and decrease of indicators of cellular toxicity and the increase of natural antioxidant enzymes, tDCS demonstrated considerable promise for avoiding DOX-induced neurotoxicity.
dc.identifier.doi10.1134/s1819712425700205
dc.identifier.eissn1819-7132
dc.identifier.endpage184
dc.identifier.issn1819-7124
dc.identifier.issue2
dc.identifier.startpage179
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/17062
dc.identifier.volume19
dc.identifier.wosWOS:001536570100010
dc.language.isoen
dc.publisherPLEIADES PUBLISHING LTD
dc.relation.ispartofNEUROCHEMICAL JOURNAL
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectdoxorubicin
dc.subjecttDCS
dc.subjectinflammation
dc.subjectoxidative stress
dc.subjectbehavior
dc.subjectDIRECT-CURRENT STIMULATION
dc.subjectTRANSCRANIAL MAGNETIC STIMULATION
dc.subjectCLINICAL-TRIAL
dc.subjectMECHANISMS
dc.subjectPAIN
dc.subjectNeurosciences
dc.subjectNeurosciences & Neurology
dc.titlePossible Neuroprotective Effect of tDCS on Doxorubicin-Induced Neurotoxicity in Rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.wos0
rdl.source.indexWOS
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)