Amelioration of diethylnitrosamine-induced acute brain injury by α-eudesmol and β-eudesmol

YILDIZ DENİZ G., GEYİKOĞLU F.

Toxicon, cilt.266, 2025 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 266
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1016/j.toxicon.2025.108550
  • Dergi Adı: Toxicon
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Aerospace Database, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, Communication Abstracts, Environment Index, Metadex, Pollution Abstracts, Veterinary Science Database, Civil Engineering Abstracts
  • Anahtar Kelimeler: Brain injury, Diethylnitrosamine, Dopamine, α-eudesmol, β-eudesmol
  • Atatürk Üniversitesi Adresli: Evet

Özet

Diethylnitrosamine (DEN) is a widely distributed environmental pollutant known for its toxicity and carcinogenicity in various animal species. The aim of the study was to investigate the neuroprotective effects of α-eudesmol and β-eudesmol against DEN-induced brain damage in rats. Sprague-Dawley rats received a single intraperitoneal dose of DEN (200 mg/kg), followed by intravenous administration of α-eudesmol or β-eudesmol (1 mg/kg) three times weekly for 21 days. Brain tissues were collected for histological, biochemical, and immunohistochemical analyses, including markers of brain injury (c-fos) and apoptosis (caspase 3). DEN exposure significantly decreased antioxidant enzyme activities (catalase, glutathione peroxidase, and superoxide dismutase) and increased oxidative stress marker malondialdehyde. It also triggered platelet activation, inflammatory cytokine production, and pathological changes in brain tissue, accompanied by upregulated c-fos and caspase 3 expression. Treatment with α-eudesmol and β-eudesmol effectively mitigated these alterations by modulating the NF-κB/COX-2/TNF-α/IL-6 signaling pathways and restoring dopamine levels to near control values. These findings highlight the potential of α-eudesmol and β-eudesmol as therapeutic agents against DEN-induced neurotoxicity.