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<p>This study aimed to investigate the histopathological and biochemical neuroprotective effects of IL-1 receptor antagonist (anakinra) administration in an asphyxia-induced cardiac arrest model. A total of 24 Wistar albino rats were randomized into three groups: control, sham (cardiac arrest + saline), and anakinra (cardiac arrest + 50&#xa0;mg/kg anakinra). Brain tissues were evaluated using a six-parameter semi-quantitative histopathological scoring system, and the composite damage score (CDS) was calculated (0–12). Levels of antioxidant and oxidative markers SOD, CAT, GSH, and MDA were analyzed spectrophotometrically. In the anakinra-treated group, neuronal degeneration, gliosis, and neuropil edema levels were significantly lower compared to the sham group (<i>p</i> &lt; 0.01 for all). Although vascular congestion and perivascular edema were observed to be lower in the anakinra group, this reduction was not statistically significant in score analyses compared to the sham group (<i>p</i> &gt; 0.05). No significant difference was found between the groups in terms of PMNL infiltration. In biochemical analyses, SOD, CAT, and GSH levels were found to be significantly higher in the anakinra group compared to both the sham and control groups (<i>p</i> &lt; 0.001), while MDA levels were significantly lower (<i>p</i> &lt; 0.001). These findings indicate that anakinra reduces oxidative stress and significantly alleviates neurohistopathological damage in the experimental model. Anakinra administration significantly reduced short-term hypoxic-ischemic brain damage following cardiac arrest, both in terms of histopathological and oxidative stress parameters. The findings suggest that targeting the IL-1-mediated inflammatory response could be an important neuroprotective approach; however, further studies are needed regarding dose, timing of administration, and long-term neurological function.</p>

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Neuroprotective effects of Interleukin-1 receptor antagonism after cardiac arrest: an experimental rat study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月16日

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  • Bilal Arslan,
  • Fatma Ayaz Yalınkılıç,
  • Adnan Erseçkin,
  • Burhan Beger,
  • Bilal Acar,
  • Utku Batu,
  • Mehmet Mehdi Oğuz,
  • Abdulaziz Yalınkılıç,
  • Orhan Beger,
  • Mehmet Zeki Erdem,
  • Halit Demir

摘要

This study aimed to investigate the histopathological and biochemical neuroprotective effects of IL-1 receptor antagonist (anakinra) administration in an asphyxia-induced cardiac arrest model. A total of 24 Wistar albino rats were randomized into three groups: control, sham (cardiac arrest + saline), and anakinra (cardiac arrest + 50 mg/kg anakinra). Brain tissues were evaluated using a six-parameter semi-quantitative histopathological scoring system, and the composite damage score (CDS) was calculated (0–12). Levels of antioxidant and oxidative markers SOD, CAT, GSH, and MDA were analyzed spectrophotometrically. In the anakinra-treated group, neuronal degeneration, gliosis, and neuropil edema levels were significantly lower compared to the sham group (p < 0.01 for all). Although vascular congestion and perivascular edema were observed to be lower in the anakinra group, this reduction was not statistically significant in score analyses compared to the sham group (p > 0.05). No significant difference was found between the groups in terms of PMNL infiltration. In biochemical analyses, SOD, CAT, and GSH levels were found to be significantly higher in the anakinra group compared to both the sham and control groups (p < 0.001), while MDA levels were significantly lower (p < 0.001). These findings indicate that anakinra reduces oxidative stress and significantly alleviates neurohistopathological damage in the experimental model. Anakinra administration significantly reduced short-term hypoxic-ischemic brain damage following cardiac arrest, both in terms of histopathological and oxidative stress parameters. The findings suggest that targeting the IL-1-mediated inflammatory response could be an important neuroprotective approach; however, further studies are needed regarding dose, timing of administration, and long-term neurological function.