Dexpanthenol mitigates trauma-induced lung injury by modulating RIPK1/RIPK3/MLKL-mediated necroptosis in rats

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Camas H. E., Savran M., Akın S. E., Dongel I., Yazkan R., Yildirim H. E., ...Daha Fazla

SCIENTIFIC REPORTS, cilt.16, sa.8468, ss.1-9, 2026 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 16 Sayı: 8468
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1038/s41598-026-40026-3
  • Dergi Adı: SCIENTIFIC REPORTS
  • Derginin Tarandığı İndeksler: Scopus, Science Citation Index Expanded (SCI-EXPANDED), BIOSIS, Chemical Abstracts Core, MEDLINE, Directory of Open Access Journals
  • Sayfa Sayıları: ss.1-9
  • Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
  • Süleyman Demirel Üniversitesi Adresli: Evet

Özet

Thoracic trauma (TRA) triggers inflammation, oxidative stress, apoptosis, and receptor-interacting protein kinase-1 (RIPK1)/receptor-interacting protein kinase-3 (RIPK3)/mixed lineage kinase domain like protein (MLKL)-mediated necroptosis, all of which contribute to contusion-related lung injury. Dexpanthenol (DEX) has anti-inflammatory and cytoprotective properties, yet its antinecroptotic potential in trauma-induced lung injury has not been fully elucidated. Forty male rats were randomly assigned to SHAM, TRA, TRA + DEX, and DEX groups. A 200 g cylindrical weight was dropped from a height of 100 cm, inducing TRA. Lung injury was assessed by histopathology, immunohistochemical staining for tumor necrosis factor-alpha (TNF-α) and caspase-3 (Cas-3), biochemical measurements of total oxidant status (TOS)/total antioxidant status (TAS)/oxidative stress index (OSI), and as well as mRNA expression levels of RIPK1/RIPK3/MLKL. TRA markedly increased hyperemia, edema, inflammatory infiltration, TNF-α, Cas-3, OSI, and RIPK1/RIPK3/MLKL expression (p < 0.001 for all). DEX significantly attenuated lung injury by reducing inflammatory scores, decreasing TNF-α and Cas-3 immunoreactivity, lowering OSI (p < 0.01), and suppressing RIPK1/RIPK3/MLKL gene activation (p < 0.001 for all). Although DEX did not fully normalize isolated TOS and TAS values, the OSI reduction indicates a net shift toward antioxidant balance. DEX mitigates trauma-induced lung injury through anti-inflammatory, antiapoptotic, antioxidant, and antinecroptotic mechanisms. These findings are preliminary, and dose-dependent effects and long-term outcomes should be clarified in future studies before clinical translation.