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<p>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&#xa0;g cylindrical weight was dropped from a height of 100&#xa0;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 (<i>p</i> &lt; 0.001 for all). DEX significantly attenuated lung injury by reducing inflammatory scores, decreasing TNF-α and Cas-3 immunoreactivity, lowering OSI (<i>p</i> &lt; 0.01), and suppressing RIPK1/RIPK3/MLKL gene activation (<i>p</i> &lt; 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月12日

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  • Hasan Ekrem Camas,
  • Mehtap Savran,
  • Suleyman Emre Akin,
  • Isa Dongel,
  • Rasih Yazkan,
  • Hasan Emre Yildirim,
  • Ilter Ilhan,
  • Muhammet Yusuf Tepebasi,
  • Mehmet Abdulkadir Sevuk,
  • Ozlem Ozmen

摘要

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.