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<p>A serious pathological condition known as pulmonary ischemia-reperfusion (I/R) injury can develop after procedures like cardiopulmonary bypass, pulmonary embolism, or lung transplantation. This process has a negative impact on distant organs, including the brain, and is linked to oxidative stress, apoptosis, and systemic inflammation. The purpose of this study was to assess the preventive effects of dexpanthenol (DEX) against pulmonary I/R injury-induced brain tissue damage in rats. Thirty-two male Wistar Albino rats were divided into four groups: control, IR (60&#xa0;min of reperfusion and ischemia), IR + DEX (500&#xa0;mg/kg), and DEX. After 60&#xa0;min of reperfusion, the rats were sacrificed and brain, cerebellum and hippocampus tissues were taken. Histopathological and immunohistochemical analyses were performed on brain, cerebellum and hippocampus tissues. Genetic and biochemical analyses were performed on brain tissue to evaluate oxidative stress, apoptosis and inflammation. In addition to increased expressions of Caspase-3 (CASP3), inducible nitric oxide synthase (INOS), and tumor necrosis factor alpha (TNF-α), pulmonary I/R injury markedly increased hyperemia, edema, neuronal damage, and gliosis. Biochemical studies showed lower total antioxidant status (TAS) levels and higher oxidative stress index (OSI) and total oxidant status (TOS) values. According to a genetic research, anti-apoptotic genes were downregulated whereas pro-apoptotic genes were upregulated. DEX treatment reduced histopathological damage by 60% (<i>p</i> ≤ 0.001) and decreased TNF-α expression by 45% in brain tissue compared to the IR group. Oxidative stress markers (TOS, OSI) were lowered by 35–50%, while anti-apoptotic BCL2 expression increased 2.1-fold (<i>p</i> ≤ 0.01). By lowering inflammation, oxidative stress, and apoptosis, DEX showed strong neuroprotective benefits on brain and cerebellar damage resulting from pulmonary I/R injury. According to these results, DEX might be a useful medication for treating brain damage brought on by systemic inflammation.</p>

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Dexpanthenol attenuates brain injury following pulmonary ischemia/reperfusion: modulation of oxidative stress, inflammation, and apoptotic pathways

  • 期刊论文

  • 发表日期：

    2025年7月16日

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  • Muhammet Yusuf Tepebaşi,
  • Halil Aşci,
  • Esma Selçuk,
  • Adem Milletsever,
  • Rümeysa Taner,
  • Merve Erçelik Koncak,
  • Özlem Özmen

摘要

A serious pathological condition known as pulmonary ischemia-reperfusion (I/R) injury can develop after procedures like cardiopulmonary bypass, pulmonary embolism, or lung transplantation. This process has a negative impact on distant organs, including the brain, and is linked to oxidative stress, apoptosis, and systemic inflammation. The purpose of this study was to assess the preventive effects of dexpanthenol (DEX) against pulmonary I/R injury-induced brain tissue damage in rats. Thirty-two male Wistar Albino rats were divided into four groups: control, IR (60 min of reperfusion and ischemia), IR + DEX (500 mg/kg), and DEX. After 60 min of reperfusion, the rats were sacrificed and brain, cerebellum and hippocampus tissues were taken. Histopathological and immunohistochemical analyses were performed on brain, cerebellum and hippocampus tissues. Genetic and biochemical analyses were performed on brain tissue to evaluate oxidative stress, apoptosis and inflammation. In addition to increased expressions of Caspase-3 (CASP3), inducible nitric oxide synthase (INOS), and tumor necrosis factor alpha (TNF-α), pulmonary I/R injury markedly increased hyperemia, edema, neuronal damage, and gliosis. Biochemical studies showed lower total antioxidant status (TAS) levels and higher oxidative stress index (OSI) and total oxidant status (TOS) values. According to a genetic research, anti-apoptotic genes were downregulated whereas pro-apoptotic genes were upregulated. DEX treatment reduced histopathological damage by 60% (p ≤ 0.001) and decreased TNF-α expression by 45% in brain tissue compared to the IR group. Oxidative stress markers (TOS, OSI) were lowered by 35–50%, while anti-apoptotic BCL2 expression increased 2.1-fold (p ≤ 0.01). By lowering inflammation, oxidative stress, and apoptosis, DEX showed strong neuroprotective benefits on brain and cerebellar damage resulting from pulmonary I/R injury. According to these results, DEX might be a useful medication for treating brain damage brought on by systemic inflammation.